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为了了解实验性自身免疫性葡萄膜视网膜炎(EAU)免疫致病机理,用Lewis鼠研究T淋巴细胞和肥大细胞的作用。用致敏的淋巴细胞特别是辅助性/诱异性T细胞亚群成功地转移给首次用来作实验的同系大鼠。接受了对S抗原致敏了的辅助性/诱导性T细胞的实验性自身免疫性葡萄膜视网膜炎(EAU)的大鼠充分表现了对此抗原的迟发型皮肤超敏反应但极轻微的Arthus反应。分析了环孢霉素、环磷酰胺,地塞米松等免疫抑制剂药物对S抗原免疫的鼠产生EAU的作用。通过选择性抑制对S抗原的迟发型皮肤超敏反应,说明仅有环孢霉素能完全抑制EAU的发生。这些资料说明T淋巴细胞在EAU致病机理中起主要的作用。根据在疾病发作以前,脉络膜的肥大细胞发生脱颗粒作用,说明除了淋巴细胞参与以外,脉络膜的肥大细胞也起了附带作用。
To understand the immunopathogenesis of experimental autoimmune uveoretinitis (EAU), Lewis rats were used to study the effects of T lymphocytes and mast cells. Stimulated lymphocytes, especially helper / mutagenized T cell subsets, were successfully transferred to naive, homogenous rats. Rats that received experimental autoimmune uveoretinitis (EAU) of helper / induced T cells that were sensitized to S antigen fully demonstrated the delayed type of skin hypersensitivity to this antigen but very slight Arthus reaction. The effects of cyclophosphamide, cyclophosphamide, dexamethasone and other immunosuppressant drugs on the production of EAU by S antigen-immunized mice were analyzed. By selectively inhibiting the delayed skin-type hypersensitivity to S antigen, only cyclosporine can completely inhibit the occurrence of EAU. These data indicate that T lymphocytes play a major role in the pathogenesis of EAU. According to the degranulation of the choroidal mast cells prior to the onset of the disease, choroidal mast cells play an incident role in addition to lymphocyte involvement.