116
Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
He, Xiao [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
|---|
| Übergeordnetes Werk: |
Enthalten in: The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types - McLaughlin, Richard J. ELSEVIER, 2022, the official journal of the International Cytokine Society, Oxford [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:63 ; year:2013 ; number:3 ; pages:270 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.cyto.2013.06.119 |
|---|
| Katalog-ID: |
ELV022162186 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV022162186 | ||
| 003 | DE-627 | ||
| 005 | 20230625134928.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.cyto.2013.06.119 |2 doi | |
| 028 | 5 | 2 | |a GBVA2013017000028.pica |
| 035 | |a (DE-627)ELV022162186 | ||
| 035 | |a (ELSEVIER)S1043-4666(13)00393-1 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 570 | |
| 082 | 0 | 4 | |a 570 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.83 |2 bkl | ||
| 100 | 1 | |a He, Xiao |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a 116 |
| 264 | 1 | |c 2013transfer abstract | |
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. | ||
| 520 | |a Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. | ||
| 700 | 1 | |a Dai, Hu |4 oth | |
| 700 | 1 | |a Jensen, Peter E |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a McLaughlin, Richard J. ELSEVIER |t The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |d 2022 |d the official journal of the International Cytokine Society |g Oxford [u.a.] |w (DE-627)ELV008219540 |
| 773 | 1 | 8 | |g volume:63 |g year:2013 |g number:3 |g pages:270 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.cyto.2013.06.119 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.83 |j Rheumatologie |j Orthopädie |q VZ |
| 951 | |a AR | ||
| 952 | |d 63 |j 2013 |e 3 |h 270 | ||
| 953 | |2 045F |a 570 | ||
| author_variant |
x h xh |
|---|---|
| matchkey_str |
ELV022162186 |
| hierarchy_sort_str |
2013transfer abstract |
| bklnumber |
44.83 |
| publishDate |
2013 |
| allfields |
10.1016/j.cyto.2013.06.119 doi GBVA2013017000028.pica (DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl He, Xiao verfasserin aut 116 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Dai, Hu oth Jensen, Peter E oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:270 https://doi.org/10.1016/j.cyto.2013.06.119 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 270 045F 570 |
| spelling |
10.1016/j.cyto.2013.06.119 doi GBVA2013017000028.pica (DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl He, Xiao verfasserin aut 116 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Dai, Hu oth Jensen, Peter E oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:270 https://doi.org/10.1016/j.cyto.2013.06.119 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 270 045F 570 |
| allfields_unstemmed |
10.1016/j.cyto.2013.06.119 doi GBVA2013017000028.pica (DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl He, Xiao verfasserin aut 116 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Dai, Hu oth Jensen, Peter E oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:270 https://doi.org/10.1016/j.cyto.2013.06.119 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 270 045F 570 |
| allfieldsGer |
10.1016/j.cyto.2013.06.119 doi GBVA2013017000028.pica (DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl He, Xiao verfasserin aut 116 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Dai, Hu oth Jensen, Peter E oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:270 https://doi.org/10.1016/j.cyto.2013.06.119 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 270 045F 570 |
| allfieldsSound |
10.1016/j.cyto.2013.06.119 doi GBVA2013017000028.pica (DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 44.83 bkl He, Xiao verfasserin aut 116 2013transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. Dai, Hu oth Jensen, Peter E oth Enthalten in Elsevier McLaughlin, Richard J. ELSEVIER The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types 2022 the official journal of the International Cytokine Society Oxford [u.a.] (DE-627)ELV008219540 volume:63 year:2013 number:3 pages:270 https://doi.org/10.1016/j.cyto.2013.06.119 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.83 Rheumatologie Orthopädie VZ AR 63 2013 3 270 045F 570 |
| language |
English |
| source |
Enthalten in The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types Oxford [u.a.] volume:63 year:2013 number:3 pages:270 |
| sourceStr |
Enthalten in The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types Oxford [u.a.] volume:63 year:2013 number:3 pages:270 |
| format_phy_str_mv |
Article |
| bklname |
Rheumatologie Orthopädie |
| institution |
findex.gbv.de |
| dewey-raw |
570 |
| isfreeaccess_bool |
false |
| container_title |
The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
| authorswithroles_txt_mv |
He, Xiao @@aut@@ Dai, Hu @@oth@@ Jensen, Peter E @@oth@@ |
| publishDateDaySort_date |
2013-01-01T00:00:00Z |
| hierarchy_top_id |
ELV008219540 |
| dewey-sort |
3570 |
| id |
ELV022162186 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV022162186</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625134928.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cyto.2013.06.119</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013017000028.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV022162186</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1043-4666(13)00393-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.83</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">He, Xiao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">116</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dai, Hu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jensen, Peter E</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">McLaughlin, Richard J. ELSEVIER</subfield><subfield code="t">The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types</subfield><subfield code="d">2022</subfield><subfield code="d">the official journal of the International Cytokine Society</subfield><subfield code="g">Oxford [u.a.]</subfield><subfield code="w">(DE-627)ELV008219540</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:63</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:270</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cyto.2013.06.119</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.83</subfield><subfield code="j">Rheumatologie</subfield><subfield code="j">Orthopädie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">63</subfield><subfield code="j">2013</subfield><subfield code="e">3</subfield><subfield code="h">270</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
| author |
He, Xiao |
| spellingShingle |
He, Xiao ddc 570 ddc 610 bkl 44.83 116 |
| authorStr |
He, Xiao |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV008219540 |
| format |
electronic Article |
| dewey-ones |
570 - Life sciences; biology 610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
570 570 DE-600 610 VZ 44.83 bkl 116 |
| topic |
ddc 570 ddc 610 bkl 44.83 |
| topic_unstemmed |
ddc 570 ddc 610 bkl 44.83 |
| topic_browse |
ddc 570 ddc 610 bkl 44.83 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
h d hd p e j pe pej |
| hierarchy_parent_title |
The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
| hierarchy_parent_id |
ELV008219540 |
| dewey-tens |
570 - Life sciences; biology 610 - Medicine & health |
| hierarchy_top_title |
The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV008219540 |
| title |
116 |
| ctrlnum |
(DE-627)ELV022162186 (ELSEVIER)S1043-4666(13)00393-1 |
| title_full |
116 |
| author_sort |
He, Xiao |
| journal |
The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
| journalStr |
The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
500 - Science 600 - Technology |
| recordtype |
marc |
| publishDateSort |
2013 |
| contenttype_str_mv |
zzz |
| container_start_page |
270 |
| author_browse |
He, Xiao |
| container_volume |
63 |
| class |
570 570 DE-600 610 VZ 44.83 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
He, Xiao |
| doi_str_mv |
10.1016/j.cyto.2013.06.119 |
| dewey-full |
570 610 |
| title_sort |
116 |
| title_auth |
116 |
| abstract |
Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. |
| abstractGer |
Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. |
| abstract_unstemmed |
Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| container_issue |
3 |
| title_short |
116 |
| url |
https://doi.org/10.1016/j.cyto.2013.06.119 |
| remote_bool |
true |
| author2 |
Dai, Hu Jensen, Peter E |
| author2Str |
Dai, Hu Jensen, Peter E |
| ppnlink |
ELV008219540 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth |
| doi_str |
10.1016/j.cyto.2013.06.119 |
| up_date |
2024-07-06T21:18:59.032Z |
| _version_ |
1803866067733315584 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV022162186</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625134928.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cyto.2013.06.119</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013017000028.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV022162186</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1043-4666(13)00393-1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.83</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">He, Xiao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">116</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Natural T regulatory cells (nTreg) are an important subpopulation of CD4+ T cells generated in thymus, and essential in preventing autoimmune diseases. However, the role of MHC-class-II-mediated TCR signaling in nTreg development remains unclear, since nTreg still presents in MHC-class-II gene knock-out mice. We examined nTreg development in Helper Deficient (HD) mice, in which the majority of MHC-class-II-restricted, CD4 lineage designated T cells is mis-directed to the CD8 lineage due to a mutated zbtb7b/ThPOK, a key regulator of CD4+ cell development, gene. In HD, both percentage and number of conventional CD4+ T cells were reduced 10 folds, compared to wild-type littermates, but the total T cell number remained unchanged since >90% of MHC-class-II restricted CD4 T cells were mis-directed to develop as CD8+ cells. Unexpectedly, the percentage of FoxP3+ cells within the residual CD4+ T cells in HD was increased to >50% in spleen and lymph nodes, compared to 5–10% of CD4+ T cells in control mice, but the absolute numbers of FoxP3+CD4+ T cells was decreased by >50% in HD. In contrast, FoxP3+CD8+ cells, both percentage and numbers, were not significantly changed in HD. Similarly, there was no increase of re-directed FoxP3+CD8+ T cells in Beta-2-microglobulin KO x HD double mutants. Furthermore, after crossing HD with a FoxP3-EGFP reporter line, >90% EGFP+ T cells were CD4+ cells, with 1% detected EGFP+CD8+ cells. Functionally, the CD4+EGFP+ T cells isolated from HD inhibited TCR-triggered IL-2 production and CD69 up-regulation of CD4+EGFP− T cells. In summary, we demonstrated that, in contrast to MHC-class-II-restricted, conventional CD4 designated T cells are mis-directed to CD8 lineage, there is no re-directed CD8 nTreg developed in HD. Our data indicates that either commitment of MHC-class-II-restricted nTreg is earlier than conventional MHC-class-II-restricted CD4+ cells or selection/expansion of MHC-class-II-restricted nTreg is not supported in CD8+ T cells.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dai, Hu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jensen, Peter E</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">McLaughlin, Richard J. ELSEVIER</subfield><subfield code="t">The minimal clinically important differences of the Simple Shoulder Test are different for different arthroplasty types</subfield><subfield code="d">2022</subfield><subfield code="d">the official journal of the International Cytokine Society</subfield><subfield code="g">Oxford [u.a.]</subfield><subfield code="w">(DE-627)ELV008219540</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:63</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:270</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cyto.2013.06.119</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.83</subfield><subfield code="j">Rheumatologie</subfield><subfield code="j">Orthopädie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">63</subfield><subfield code="j">2013</subfield><subfield code="e">3</subfield><subfield code="h">270</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
| score |
7.3982153 |