Influence of CD4 or CD8 deficiency on collagen-induced arthritis
Influence of CD4 or CD8 deficiency on collagen-induced arthritis
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DOI：
10.1046/j.1365-2567.2001.01257.x
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发表时间：
2001-07-01
期刊：
影响因子：
6.4
通讯作者：
Holmdahl, R
中科院分区：
文献类型：
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作者：
Ehinger, M;Vestberg, M;Holmdahl, R
T细胞在类风湿性关节炎的小鼠胶原诱导的关节炎（CIA）模型中的作用尚未阐明，并且关于CD 4和CD 8 T细胞的作用已经报道了不同的结果。为了解决这个问题，我们研究了CD 4或CD 8缺陷的B10.Q小鼠。缺乏CD 4的小鼠对疾病的易感性较低，但不完全抵抗，而CD 8缺乏对疾病没有显着影响。未观察到晚期复发的发展差异。有趣的是，CD 4缺陷小鼠对免疫显性II型胶原（CII）256-270肽的糖基化形式的应答严重降低，而对非糖基化肽的应答没有显著差异。此外，CD 4缺陷小鼠对CII的抗体应答较低，解释了较低的疾病易感性。与以前报道的结果相比，很明显，缺乏CD 4分子对CIA有不同的影响。如果存在于不同的遗传背景中，则可能与不同小鼠品系中CIA不同疾病途径的发生相关的发现。
The role of T cells in the mouse collagen-induced arthritis (CIA) model for rheumatoid arthritis is not clarified, and different results have been reported concerning the role of CD4 and CD8 T cells. To address this issue, we have investigated B10.Q mice deficient for CD4 or CD8. The mice lacking CD4 were found to be less susceptible to disease, but not completely resistant, whereas the CD8 deficiency had no significant impact on the disease. No difference in the development of late occurring relapses was noted. Interestingly, the CD4-deficient mice had a severely reduced response to the glycosylated form of the immunodominant type II collagen (CII) 256-270 peptide whereas the response to the non-glycosylated peptide was not significantly different. Furthermore, CD4-deficient mice had lower antibody responses to CII, explaining the lower disease susceptibility. In comparison with previously reported results, it is apparent that the lack of CD4 molecules has a different impact on CIA. if present on different genetic backgrounds, findings that could possibly be related to the occurrence of different disease pathways of CIA in different mouse strains.