Adoptive transfer of experimental autoimmune uveoretinitis in rats. Immunopathogenic mechanisms and histologic features.
Adoptive transfer of experimental autoimmune uveoretinitis in rats. Immunopathogenic mechanisms and histologic features.
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发表时间：
1985
影响因子：
4.4
通讯作者：
M. Mochizuki;T. Kuwabara;C. Mcallister;R. Nussenblatt;I. Gery
中科院分区：
文献类型：
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作者：
M. Mochizuki;T. Kuwabara;C. Mcallister;R. Nussenblatt;I. Gery
为了了解实验性自身免疫性葡萄膜视网膜炎（EAU）的免疫致病机制，研究了淋巴细胞转移疾病的能力。将s抗原免疫大鼠的脾脏或淋巴结（LN）细胞与s抗原或豆豆蛋白A （Con A）培养后，通过腹腔注射将EAU转移到幼稚的同基因大鼠。相比之下，同样的细胞在玻璃体内注射时不会引起受体眼睛的炎症变化。通过单克隆抗体富集淋巴细胞亚群来确定转移EAU的淋巴细胞的身份。EAU可以通过辅助/诱导t细胞亚群转移，而不能通过抑制/细胞毒性t细胞亚群转移。s抗原培养的脾脏或LN细胞受体大鼠对s抗原表现出体液和细胞免疫反应。另一方面，经Con A培养的脾细胞受体仅对s抗原产生细胞免疫应答。然而，这两组受援国都充分发展了EAU。受体大鼠的临床和组织学变化与主动免疫诱导的大鼠非常相似。严重的组织损伤发生在感光细胞层，但炎症浸润也见于眼部其他组织。甚至在没有检测到s抗原抗体的受者的眼睛中，整个眼部组织都发现了多形核白细胞（PMNs）的浸润，这表明大鼠眼部PMNs的浸润不一定是关节炎样炎症过程的结果。
In order to learn about the immunopathogenic mechanisms of experimental autoimmune uveoretinitis (EAU), the capacity of lymphocytes to transfer the disease was studied. EAU was transferred to naive syngeneic rats by intraperitoneal injection of spleen or lymph node (LN) cells from S-antigen immunized rats, following their incubation in culture with either S-antigen or concanavalin A (Con A). In contrast, the same cells did not cause inflammatory changes in the recipient eyes when injected intravitreally. The identity of the lymphocytes that transfer EAU was determined by using monoclonal antibody enriched subsets of lymphocytes. EAU was transferred by the subset of helper/inducer T-cells, but not by T-cells of the suppressor/cytotoxic subset. Recipient rats of spleen or LN cells cultured with S-antigen exhibited both humoral and cellular immune responses to S-antigen. On the other hand, recipients of spleen cells cultured with Con A developed only cellular immune response to S-antigen. Yet, both groups of recipients fully developed EAU. The clinical and histologic changes in recipient rats closely resembled those in rats in which EAU was induced by active immunization. Severe tissue damage occurred at the photoreceptor cell layer, but inflammatory infiltration also was found in other ocular tissues. Involvement of polymorphonuclear leukocytes (PMNs) was noted throughout ocular tissues even in the eyes of recipients with no detectable antibodies to S-antigen, suggesting that the ocular PMNs infiltration in rats is not necessarily the result of an Arthus-like inflammatory process.