Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide
Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphat...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Iwanami, Keiichi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Anmerkung: |
© Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: Arthritis Research & Therapy - London : BioMed Central, 1999, 11(2009), 6 vom: 09. Nov. |
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| Übergeordnetes Werk: |
volume:11 ; year:2009 ; number:6 ; day:09 ; month:11 |
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| DOI / URN: |
10.1186/ar2854 |
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| Katalog-ID: |
SPR030832632 |
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| 245 | 1 | 0 | |a Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide |
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| 520 | |a Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. | ||
| 650 | 4 | |a Rheumatoid Arthritis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tocilizumab |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Altered Peptide Ligand |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Matsumoto, Isao |4 aut | |
| 700 | 1 | |a Yoshiga, Yohei |4 aut | |
| 700 | 1 | |a Inoue, Asuka |4 aut | |
| 700 | 1 | |a Kondo, Yuya |4 aut | |
| 700 | 1 | |a Yamamoto, Kayo |4 aut | |
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| 700 | 1 | |a Minami, Reiko |4 aut | |
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| 700 | 1 | |a Ito, Satoshi |4 aut | |
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| 700 | 1 | |a Sumida, Takayuki |4 aut | |
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10.1186/ar2854 doi (DE-627)SPR030832632 (SPR)ar2854-e DE-627 ger DE-627 rakwb eng Iwanami, Keiichi verfasserin aut Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. Rheumatoid Arthritis (dpeaa)DE-He213 Tocilizumab (dpeaa)DE-He213 Analog Peptide (dpeaa)DE-He213 Experimental Autoimmune Encephalitis (dpeaa)DE-He213 Altered Peptide Ligand (dpeaa)DE-He213 Matsumoto, Isao aut Yoshiga, Yohei aut Inoue, Asuka aut Kondo, Yuya aut Yamamoto, Kayo aut Tanaka, Yoko aut Minami, Reiko aut Hayashi, Taichi aut Goto, Daisuke aut Ito, Satoshi aut Nishimura, Yasuharu aut Sumida, Takayuki aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 6 vom: 09. Nov. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:6 day:09 month:11 https://dx.doi.org/10.1186/ar2854 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 6 09 11 |
| spelling |
10.1186/ar2854 doi (DE-627)SPR030832632 (SPR)ar2854-e DE-627 ger DE-627 rakwb eng Iwanami, Keiichi verfasserin aut Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. Rheumatoid Arthritis (dpeaa)DE-He213 Tocilizumab (dpeaa)DE-He213 Analog Peptide (dpeaa)DE-He213 Experimental Autoimmune Encephalitis (dpeaa)DE-He213 Altered Peptide Ligand (dpeaa)DE-He213 Matsumoto, Isao aut Yoshiga, Yohei aut Inoue, Asuka aut Kondo, Yuya aut Yamamoto, Kayo aut Tanaka, Yoko aut Minami, Reiko aut Hayashi, Taichi aut Goto, Daisuke aut Ito, Satoshi aut Nishimura, Yasuharu aut Sumida, Takayuki aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 6 vom: 09. Nov. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:6 day:09 month:11 https://dx.doi.org/10.1186/ar2854 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 6 09 11 |
| allfields_unstemmed |
10.1186/ar2854 doi (DE-627)SPR030832632 (SPR)ar2854-e DE-627 ger DE-627 rakwb eng Iwanami, Keiichi verfasserin aut Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. Rheumatoid Arthritis (dpeaa)DE-He213 Tocilizumab (dpeaa)DE-He213 Analog Peptide (dpeaa)DE-He213 Experimental Autoimmune Encephalitis (dpeaa)DE-He213 Altered Peptide Ligand (dpeaa)DE-He213 Matsumoto, Isao aut Yoshiga, Yohei aut Inoue, Asuka aut Kondo, Yuya aut Yamamoto, Kayo aut Tanaka, Yoko aut Minami, Reiko aut Hayashi, Taichi aut Goto, Daisuke aut Ito, Satoshi aut Nishimura, Yasuharu aut Sumida, Takayuki aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 6 vom: 09. Nov. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:6 day:09 month:11 https://dx.doi.org/10.1186/ar2854 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 6 09 11 |
| allfieldsGer |
10.1186/ar2854 doi (DE-627)SPR030832632 (SPR)ar2854-e DE-627 ger DE-627 rakwb eng Iwanami, Keiichi verfasserin aut Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. Rheumatoid Arthritis (dpeaa)DE-He213 Tocilizumab (dpeaa)DE-He213 Analog Peptide (dpeaa)DE-He213 Experimental Autoimmune Encephalitis (dpeaa)DE-He213 Altered Peptide Ligand (dpeaa)DE-He213 Matsumoto, Isao aut Yoshiga, Yohei aut Inoue, Asuka aut Kondo, Yuya aut Yamamoto, Kayo aut Tanaka, Yoko aut Minami, Reiko aut Hayashi, Taichi aut Goto, Daisuke aut Ito, Satoshi aut Nishimura, Yasuharu aut Sumida, Takayuki aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 6 vom: 09. Nov. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:6 day:09 month:11 https://dx.doi.org/10.1186/ar2854 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 6 09 11 |
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10.1186/ar2854 doi (DE-627)SPR030832632 (SPR)ar2854-e DE-627 ger DE-627 rakwb eng Iwanami, Keiichi verfasserin aut Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. Rheumatoid Arthritis (dpeaa)DE-He213 Tocilizumab (dpeaa)DE-He213 Analog Peptide (dpeaa)DE-He213 Experimental Autoimmune Encephalitis (dpeaa)DE-He213 Altered Peptide Ligand (dpeaa)DE-He213 Matsumoto, Isao aut Yoshiga, Yohei aut Inoue, Asuka aut Kondo, Yuya aut Yamamoto, Kayo aut Tanaka, Yoko aut Minami, Reiko aut Hayashi, Taichi aut Goto, Daisuke aut Ito, Satoshi aut Nishimura, Yasuharu aut Sumida, Takayuki aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 6 vom: 09. Nov. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:6 day:09 month:11 https://dx.doi.org/10.1186/ar2854 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 6 09 11 |
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Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide |
| abstract |
Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Introduction Immunosuppressants, including anti-TNFα antibodies, have remarkable effects in rheumatoid arthritis; however, they increase infectious events. The present study was designed to examine the effects and immunological change of action of altered peptide ligands (APLs) on glucose-6-phosphate isomerase (GPI) peptide-induced arthritis. Methods DBA/1 mice were immunized with $ hGPI_{325-339} $, and cells of draining lymph node (DLN) were stimulated with $ hGPI_{325-339} $ to investigate the T-cell receptor (TCR) repertoire of antigen-specific $ CD4^{+} $ T cells by flow cytometry. Twenty types of APLs with one amino acid substitution at a TCR contact site of $ hGPI_{325-339} $ were synthesized. $ CD4^{+} $ T cells primed with human GPI and antigen-presenting cells were co-cultured with each APL and cytokine production was measured by ELISA to identify antagonistic APLs. Antagonistic APLs were co-immunized with $ hGPI_{325-339} $ to investigate whether arthritis could be antigen-specifically inhibited by APL. After co-immunization, DLN cells were stimulated with $ hGPI_{325-339} $ or APL to investigate Th17 and regulatory T-cell population by flow cytometry, and anti-mouse GPI antibodies were measured by ELISA. Results Human $ GPI_{325-339} $-specific Th17 cells showed predominant usage of TCRVβ8.1 8.2. Among the 20 synthesized APLs, four (APL 6; N329S, APL 7; N329T, APL 12; G332A, APL 13; G332V) significantly reduced IL-17 production by $ CD4^{+} $ T cells in the presence of $ hGPI_{325-339} $. Co-immunization with each antagonistic APL markedly prevented the development of arthritis, especially APL 13 (G332V). Although co-immunization with APL did not affect the population of Th17 and regulatory T cells, the titers of anti-mouse GPI antibodies in mice co-immunized with APL were significantly lower than in those without APL. Conclusions We prepared antagonistic APLs that antigen-specifically inhibited the development of experimental arthritis. Understanding the inhibitory mechanisms of APLs may pave the way for the development of novel therapies for arthritis induced by autoimmune responses to ubiquitous antigens. © Iwanami et al.; licensee BioMed Central Ltd. 2009. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( |
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Altered peptide ligands inhibit arthritis induced by glucose-6-phosphate isomerase peptide |
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Matsumoto, Isao Yoshiga, Yohei Inoue, Asuka Kondo, Yuya Yamamoto, Kayo Tanaka, Yoko Minami, Reiko Hayashi, Taichi Goto, Daisuke Ito, Satoshi Nishimura, Yasuharu Sumida, Takayuki |
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Matsumoto, Isao Yoshiga, Yohei Inoue, Asuka Kondo, Yuya Yamamoto, Kayo Tanaka, Yoko Minami, Reiko Hayashi, Taichi Goto, Daisuke Ito, Satoshi Nishimura, Yasuharu Sumida, Takayuki |
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