Takagishi K, Kaibara N, Hotokebuchi T, Arita C, Morinaga M, Arai K
J Immunol. 1985 Jun;134(6):3864-7.
The role of cellular immunity in collagen arthritis was investigated with congenitally athymic nude rats (rnu/rnu) and their heterozygous littermates (rnu/+). Immunization with type II collagen induced polyarthritis and definite immunity to type II collagen in rnu/+ rats, whereas rnu/rnu rats did not develop arthritis or immunity to collagen. An additional study demonstrated that collagen arthritis could be passively transferred with a serum concentrate from arthritic Sprague-Dawley rats to naive rnu/rnu rats as well as to rnu/+ rats. Histopathologically, the passively transferred arthritis in rnu/rnu rats resembled that in rnu/+ rats. Despite no difference in clearance of anti-type II collagen antibody after transfer between them, the passively transferred arthritis in rnu/rnu rats was significantly enhanced and prolonged in comparison with that in rnu/+ rats. These results indicate that arthritis may be inducible by humoral immunity in the absence of functional T cells and also suggest that anti-type II collagen-antibody is not the sole regulatory factor and that the suppressor cell system might regulate the clinical course of the disease.
利用先天性无胸腺裸鼠(rnu/rnu)及其杂合子同窝仔鼠(rnu/+)研究了细胞免疫在胶原性关节炎中的作用。用Ⅱ型胶原免疫可使rnu/+大鼠发生多关节炎并对Ⅱ型胶原产生明确的免疫反应,而rnu/rnu大鼠既不发生关节炎也不产生对胶原的免疫反应。另一项研究表明,胶原性关节炎可通过将来自患有关节炎的斯普拉格-道利大鼠的血清浓缩物被动转移至未接触过抗原的rnu/rnu大鼠以及rnu/+大鼠体内而引发。组织病理学检查显示,rnu/rnu大鼠中被动转移的关节炎与rnu/+大鼠中的相似。尽管二者之间在转移后抗Ⅱ型胶原抗体的清除方面没有差异,但与rnu/+大鼠相比,rnu/rnu大鼠中被动转移的关节炎显著加重且持续时间延长。这些结果表明,在缺乏功能性T细胞的情况下,体液免疫可能诱导关节炎发生,同时也提示抗Ⅱ型胶原抗体不是唯一的调节因子,抑制细胞系统可能调节该疾病的临床病程。