Ehinger M, Vestberg M, Johansson A C, Johannesson M, Svensson A, Holmdahl R
Department of Molecular Biophysics and Medical Inflammation Research Center for Chemistry and Chemical Engineering, Lund University, Lund, Sweden.
Immunology. 2001 Jul;103(3):291-300. doi: 10.1046/j.1365-2567.2001.01257.x.
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.
T细胞在类风湿关节炎的小鼠胶原诱导性关节炎(CIA)模型中的作用尚未明确,关于CD4和CD8 T细胞的作用也有不同的报道。为解决这一问题,我们研究了缺乏CD4或CD8的B10.Q小鼠。发现缺乏CD4的小鼠对疾病的易感性较低,但并非完全抵抗,而缺乏CD8对疾病没有显著影响。晚期复发的发生没有差异。有趣的是,缺乏CD4的小鼠对免疫显性II型胶原(CII)256 - 270糖基化肽的反应严重降低,而对非糖基化肽的反应没有显著差异。此外,缺乏CD4的小鼠对CII的抗体反应较低,这解释了其较低的疾病易感性。与先前报道的结果相比,显然如果存在于不同的遗传背景中,CD4分子的缺失对CIA有不同的影响,这些发现可能与不同小鼠品系中CIA不同疾病途径的发生有关。