CXCR3, CXCL10 and type 1 diabetes
Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different au...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Antonelli, Alessandro [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2014transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
9 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study - Lee, Myung Kyung ELSEVIER, 2021, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:25 ; year:2014 ; number:1 ; pages:57-65 ; extent:9 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.cytogfr.2014.01.006 |
|---|
| Katalog-ID: |
ELV039505014 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV039505014 | ||
| 003 | DE-627 | ||
| 005 | 20230625225107.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2014 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.cytogfr.2014.01.006 |2 doi | |
| 028 | 5 | 2 | |a GBVA2014019000009.pica |
| 035 | |a (DE-627)ELV039505014 | ||
| 035 | |a (ELSEVIER)S1359-6101(14)00007-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.81 |2 bkl | ||
| 084 | |a 44.63 |2 bkl | ||
| 100 | 1 | |a Antonelli, Alessandro |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a CXCR3, CXCL10 and type 1 diabetes |
| 264 | 1 | |c 2014transfer abstract | |
| 300 | |a 9 | ||
| 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 Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. | ||
| 520 | |a Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. | ||
| 650 | 7 | |a CXCL10 |2 Elsevier | |
| 650 | 7 | |a Cytokines |2 Elsevier | |
| 650 | 7 | |a Type 1 diabetes |2 Elsevier | |
| 650 | 7 | |a CXCR3 |2 Elsevier | |
| 650 | 7 | |a Viral infections |2 Elsevier | |
| 700 | 1 | |a Ferrari, Silvia Martina |4 oth | |
| 700 | 1 | |a Corrado, Alda |4 oth | |
| 700 | 1 | |a Ferrannini, Ele |4 oth | |
| 700 | 1 | |a Fallahi, Poupak |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Lee, Myung Kyung ELSEVIER |t Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |d 2021 |g Amsterdam [u.a.] |w (DE-627)ELV007431309 |
| 773 | 1 | 8 | |g volume:25 |g year:2014 |g number:1 |g pages:57-65 |g extent:9 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.cytogfr.2014.01.006 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 936 | b | k | |a 44.81 |j Onkologie |q VZ |
| 936 | b | k | |a 44.63 |j Krankenpflege |q VZ |
| 951 | |a AR | ||
| 952 | |d 25 |j 2014 |e 1 |h 57-65 |g 9 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
a a aa |
|---|---|
| matchkey_str |
antonellialessandroferrarisilviamartinac:2014----:xrcc1adye |
| hierarchy_sort_str |
2014transfer abstract |
| bklnumber |
44.81 44.63 |
| publishDate |
2014 |
| allfields |
10.1016/j.cytogfr.2014.01.006 doi GBVA2014019000009.pica (DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl Antonelli, Alessandro verfasserin aut CXCR3, CXCL10 and type 1 diabetes 2014transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier Ferrari, Silvia Martina oth Corrado, Alda oth Ferrannini, Ele oth Fallahi, Poupak oth Enthalten in Elsevier Science Lee, Myung Kyung ELSEVIER Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study 2021 Amsterdam [u.a.] (DE-627)ELV007431309 volume:25 year:2014 number:1 pages:57-65 extent:9 https://doi.org/10.1016/j.cytogfr.2014.01.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.81 Onkologie VZ 44.63 Krankenpflege VZ AR 25 2014 1 57-65 9 045F 610 |
| spelling |
10.1016/j.cytogfr.2014.01.006 doi GBVA2014019000009.pica (DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl Antonelli, Alessandro verfasserin aut CXCR3, CXCL10 and type 1 diabetes 2014transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier Ferrari, Silvia Martina oth Corrado, Alda oth Ferrannini, Ele oth Fallahi, Poupak oth Enthalten in Elsevier Science Lee, Myung Kyung ELSEVIER Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study 2021 Amsterdam [u.a.] (DE-627)ELV007431309 volume:25 year:2014 number:1 pages:57-65 extent:9 https://doi.org/10.1016/j.cytogfr.2014.01.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.81 Onkologie VZ 44.63 Krankenpflege VZ AR 25 2014 1 57-65 9 045F 610 |
| allfields_unstemmed |
10.1016/j.cytogfr.2014.01.006 doi GBVA2014019000009.pica (DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl Antonelli, Alessandro verfasserin aut CXCR3, CXCL10 and type 1 diabetes 2014transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier Ferrari, Silvia Martina oth Corrado, Alda oth Ferrannini, Ele oth Fallahi, Poupak oth Enthalten in Elsevier Science Lee, Myung Kyung ELSEVIER Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study 2021 Amsterdam [u.a.] (DE-627)ELV007431309 volume:25 year:2014 number:1 pages:57-65 extent:9 https://doi.org/10.1016/j.cytogfr.2014.01.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.81 Onkologie VZ 44.63 Krankenpflege VZ AR 25 2014 1 57-65 9 045F 610 |
| allfieldsGer |
10.1016/j.cytogfr.2014.01.006 doi GBVA2014019000009.pica (DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl Antonelli, Alessandro verfasserin aut CXCR3, CXCL10 and type 1 diabetes 2014transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier Ferrari, Silvia Martina oth Corrado, Alda oth Ferrannini, Ele oth Fallahi, Poupak oth Enthalten in Elsevier Science Lee, Myung Kyung ELSEVIER Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study 2021 Amsterdam [u.a.] (DE-627)ELV007431309 volume:25 year:2014 number:1 pages:57-65 extent:9 https://doi.org/10.1016/j.cytogfr.2014.01.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.81 Onkologie VZ 44.63 Krankenpflege VZ AR 25 2014 1 57-65 9 045F 610 |
| allfieldsSound |
10.1016/j.cytogfr.2014.01.006 doi GBVA2014019000009.pica (DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl Antonelli, Alessandro verfasserin aut CXCR3, CXCL10 and type 1 diabetes 2014transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier Ferrari, Silvia Martina oth Corrado, Alda oth Ferrannini, Ele oth Fallahi, Poupak oth Enthalten in Elsevier Science Lee, Myung Kyung ELSEVIER Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study 2021 Amsterdam [u.a.] (DE-627)ELV007431309 volume:25 year:2014 number:1 pages:57-65 extent:9 https://doi.org/10.1016/j.cytogfr.2014.01.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.81 Onkologie VZ 44.63 Krankenpflege VZ AR 25 2014 1 57-65 9 045F 610 |
| language |
English |
| source |
Enthalten in Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study Amsterdam [u.a.] volume:25 year:2014 number:1 pages:57-65 extent:9 |
| sourceStr |
Enthalten in Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study Amsterdam [u.a.] volume:25 year:2014 number:1 pages:57-65 extent:9 |
| format_phy_str_mv |
Article |
| bklname |
Onkologie Krankenpflege |
| institution |
findex.gbv.de |
| topic_facet |
CXCL10 Cytokines Type 1 diabetes CXCR3 Viral infections |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |
| authorswithroles_txt_mv |
Antonelli, Alessandro @@aut@@ Ferrari, Silvia Martina @@oth@@ Corrado, Alda @@oth@@ Ferrannini, Ele @@oth@@ Fallahi, Poupak @@oth@@ |
| publishDateDaySort_date |
2014-01-01T00:00:00Z |
| hierarchy_top_id |
ELV007431309 |
| dewey-sort |
3610 |
| id |
ELV039505014 |
| 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">ELV039505014</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625225107.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2014 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cytogfr.2014.01.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2014019000009.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV039505014</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1359-6101(14)00007-0</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">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</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">44.81</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.63</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Antonelli, Alessandro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CXCR3, CXCL10 and type 1 diabetes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</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">Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cytokines</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Type 1 diabetes</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCR3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Viral infections</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrari, Silvia Martina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Corrado, Alda</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrannini, Ele</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fallahi, Poupak</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Lee, Myung Kyung ELSEVIER</subfield><subfield code="t">Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study</subfield><subfield code="d">2021</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV007431309</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:25</subfield><subfield code="g">year:2014</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:57-65</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cytogfr.2014.01.006</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="936" ind1="b" ind2="k"><subfield code="a">44.81</subfield><subfield code="j">Onkologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.63</subfield><subfield code="j">Krankenpflege</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">25</subfield><subfield code="j">2014</subfield><subfield code="e">1</subfield><subfield code="h">57-65</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Antonelli, Alessandro |
| spellingShingle |
Antonelli, Alessandro ddc 610 bkl 44.81 bkl 44.63 Elsevier CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections CXCR3, CXCL10 and type 1 diabetes |
| authorStr |
Antonelli, Alessandro |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV007431309 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl CXCR3, CXCL10 and type 1 diabetes CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections Elsevier |
| topic |
ddc 610 bkl 44.81 bkl 44.63 Elsevier CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections |
| topic_unstemmed |
ddc 610 bkl 44.81 bkl 44.63 Elsevier CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections |
| topic_browse |
ddc 610 bkl 44.81 bkl 44.63 Elsevier CXCL10 Elsevier Cytokines Elsevier Type 1 diabetes Elsevier CXCR3 Elsevier Viral infections |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
s m f sm smf a c ac e f ef p f pf |
| hierarchy_parent_title |
Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |
| hierarchy_parent_id |
ELV007431309 |
| dewey-tens |
610 - Medicine & health |
| hierarchy_top_title |
Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV007431309 |
| title |
CXCR3, CXCL10 and type 1 diabetes |
| ctrlnum |
(DE-627)ELV039505014 (ELSEVIER)S1359-6101(14)00007-0 |
| title_full |
CXCR3, CXCL10 and type 1 diabetes |
| author_sort |
Antonelli, Alessandro |
| journal |
Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |
| journalStr |
Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2014 |
| contenttype_str_mv |
zzz |
| container_start_page |
57 |
| author_browse |
Antonelli, Alessandro |
| container_volume |
25 |
| physical |
9 |
| class |
610 610 DE-600 610 VZ 44.81 bkl 44.63 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Antonelli, Alessandro |
| doi_str_mv |
10.1016/j.cytogfr.2014.01.006 |
| dewey-full |
610 |
| title_sort |
cxcr3, cxcl10 and type 1 diabetes |
| title_auth |
CXCR3, CXCL10 and type 1 diabetes |
| abstract |
Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. |
| abstractGer |
Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. |
| abstract_unstemmed |
Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| container_issue |
1 |
| title_short |
CXCR3, CXCL10 and type 1 diabetes |
| url |
https://doi.org/10.1016/j.cytogfr.2014.01.006 |
| remote_bool |
true |
| author2 |
Ferrari, Silvia Martina Corrado, Alda Ferrannini, Ele Fallahi, Poupak |
| author2Str |
Ferrari, Silvia Martina Corrado, Alda Ferrannini, Ele Fallahi, Poupak |
| ppnlink |
ELV007431309 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth |
| doi_str |
10.1016/j.cytogfr.2014.01.006 |
| up_date |
2024-07-06T20:46:44.913Z |
| _version_ |
1803864039661502464 |
| 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">ELV039505014</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625225107.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2014 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.cytogfr.2014.01.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2014019000009.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV039505014</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1359-6101(14)00007-0</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">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</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">44.81</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.63</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Antonelli, Alessandro</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">CXCR3, CXCL10 and type 1 diabetes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</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">Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCL10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cytokines</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Type 1 diabetes</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CXCR3</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Viral infections</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrari, Silvia Martina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Corrado, Alda</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ferrannini, Ele</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fallahi, Poupak</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Lee, Myung Kyung ELSEVIER</subfield><subfield code="t">Decisional balance, self-leadership, self-efficacy, planning, and stages of change in adopting exercise behaviors in patients with stomach cancer: A cross-sectional study</subfield><subfield code="d">2021</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV007431309</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:25</subfield><subfield code="g">year:2014</subfield><subfield code="g">number:1</subfield><subfield code="g">pages:57-65</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.cytogfr.2014.01.006</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="936" ind1="b" ind2="k"><subfield code="a">44.81</subfield><subfield code="j">Onkologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.63</subfield><subfield code="j">Krankenpflege</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">25</subfield><subfield code="j">2014</subfield><subfield code="e">1</subfield><subfield code="h">57-65</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4007254 |