Kaibara N, Morinaga M, Arita C, Hotokebuchi T, Takagishi K
Clin Immunol Immunopathol. 1985 May;35(2):252-60. doi: 10.1016/0090-1229(85)90071-6.
Collagen arthritis has been passively transferred with a serum concentrate from immunized donors to immunologically naive recipients as well as cyclosporin-treated, type II collagen-tolerant rats. These findings point to an important role for anticollagen antibody and appear to rule out a role for cellular immunity to type II collagen in the initiation of this disease. The passively transferred arthritis was a transient lesion in the majority of naive recipients and in the cyclosporin-treated, type II collagen-tolerant rats as well when a serum concentrate was transferred after the cessation of cyclosporin treatment. When cyclosporin-treated, type II collagen-tolerant rats received transfer concentrate while cyclosporin was administered continuously, arthritis was significantly enhanced, and lasted as long as cyclosporin was administered and in the majority of rats up to 2 weeks after the cessation of cyclosporin treatment. These results, together with a rapid clearance of anticollagen antibody from the serum, suggest that anticollagen antibody is not the sole regulatory factor and that a cellular suppressor system, sensitive to cyclosporin, might participate in the regulation of this disease process.
胶原性关节炎已通过将免疫供体的血清浓缩物被动转移至免疫未接触过抗原的受体以及经环孢素治疗的、对II型胶原耐受的大鼠身上得以证实。这些发现表明抗胶原抗体起着重要作用，并且似乎排除了细胞免疫对II型胶原在该疾病起始过程中的作用。在大多数未接触过抗原的受体以及经环孢素治疗的、对II型胶原耐受的大鼠中，当在环孢素治疗停止后转移血清浓缩物时，被动转移的关节炎是一种短暂性病变。当经环孢素治疗的、对II型胶原耐受的大鼠在持续给予环孢素的同时接受转移浓缩物时，关节炎显著加重，并且只要给予环孢素就会持续存在，在大多数大鼠中直至环孢素治疗停止后2周。这些结果，连同抗胶原抗体从血清中的快速清除，提示抗胶原抗体不是唯一的调节因子，并且一个对环孢素敏感的细胞抑制系统可能参与了该疾病进程的调节。
