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Selective Expansion of TCR $V{\beta}3$+CD4+T Cells in Collagen-induced Arthritis in DBA/1 Mice  

Lee, Jae-Seon (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Cho, Mi-La (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Lee, Jung-Eun (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Min, So-Youn (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Yoon, Chong-Hyeon (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Kim, Wan-Uk (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Min, Jun-Ki (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Park, Sung-Hwan (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Kim, Ho-Youn (Rheumatism Research Center, Catholic Institute of Medical Science, The Catholic University of Korea)
Publication Information
IMMUNE NETWORK / v.5, no.2, 2005 , pp. 78-88 More about this Journal
Abstract
Background: Collagen-induced arthritis (CIA) in mice is animal model of autoimmune disease known as rheumatic arthritis in human. We investigated CII-specific CD4+ T cell receptor usage in CIA mice. Methods: In CIA model, draining lymph node (dLN) CD4+ T cells and splenocytes at $3^{rd},\;5^{th},\;8^{th}$ week, we investigated CII-specific T cell proliferation, production of IL-17, IFN-${\gamma}$, TNF-${\alpha}$, IL-4 and IL-10. And we also performed anti-CII IgG Ab measurements in serum level, TCRV ${\beta}$ usage and T cell clonality with RT-PCR-SSCP analysis. Also, we performed proliferative response against CII when CII-specific T cell subset is deleted. Results: CIA mice showed more increase in the serum level of anti-CII IgG than normal mice after induction of arthritis. And the level of anti-CII IgG2a in CIA mice was increased after $3^{rd}$ week after primary immunization, while anti-CII IgG1 was decreased. Draining LN CD4+ T cells have proliferated against CII stimulation at $3^{rd}$ week after $1^{st}$immunization. CD4+T cells derived from dLN of CIA mice produced proinflammatory cytokine IFN-${\gamma}$, IL-17 etc. Draining LN CD4 T cells of CIA presented higher proportion of CD4+V ${\beta}3$+subset compared to those of normal mice at $3^{rd}$ week after $1^{st}$ immunization, and they were increased in proportion by CII stimulation. Draining LN CD4+ T cells without TCRV ${\beta}3+/V{\beta}8.1/8.2+/V{\beta}$10b+cells were not responsive against CII stimulation. But, CII-reactive response of TCRV ${\beta}3-/V{\beta}8.1/8.2-/V{\beta}$10b- T cells was recovered when $V{\beta}3+$ T cells were added in culture. Conclusion: Our results indicate that CD4+$V{\beta}3+$ T cells are selectively expanded in dLN of CIA mice, and their recovery upon CII re-stimulation in vitro, as well as the production Th1-type cytokines, may play pivotal role in CIA pathogenesis.
Keywords
TCRV ${\beta}3$; antigen-specific T cell; type II collagen; collagen-induced arthritis;
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