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粘膜应用自身抗原诱导外周免疫耐受状态 ,依赖应用抗原剂量 ,诱导产生两种粘膜耐受机制 :高剂量偏向产生T细胞克隆无能 /排除 ,低剂量偏向产生分泌抑制性细胞因子(TGF β ,IL 4,IL 10 )的T细胞克隆扩增。大量研究表明鼻内或口服应用抗原诱导粘膜耐受可有效预防几种实验性自身免疫病 (EAE ,EAMG ,EAN ,EAU ,IDDM和CIA) ,在同等剂量鼻内应用比口服诱导粘膜耐受更有效。基于动物实验结果 ,对人类自身免疫病MS、RA和葡萄膜炎的临床试验正在进行。耐受原与CTB偶联可拓宽粘膜耐受的有效性 ,加强对临床疾病的抑制。然而 ,粘膜免疫与抗原应用途径、种类和疾病发病时间有关 ,可能表现为双重作用 ,尤其在发展中的自身免疫病 ,粘膜应用抗原可能加重病情。
Mucosal application of autoantigen to induce peripheral immune tolerance depends on the use of antigen dose, inducing two kinds of mucosal tolerance mechanisms: high dose biased T cell clones incompetent / excluded, low dose biased to produce secretory inhibitory cytokines (TGF β, IL 4, IL 10) T cell clones were amplified. Numerous studies have shown that intranasal or oral administration of antigen-induced mucosal tolerance can be effective in preventing several experimental autoimmune diseases (EAE, EAMG, EAN, EAU, IDDM and CIA) and that oral administration of mucosal tolerance at a comparable dose effective. Based on animal experimental results, clinical trials on human autoimmune diseases MS, RA and uveitis are underway. The combination of tolerogenic and CTB can broaden the effectiveness of mucosal tolerance and enhance the inhibition of clinical disease. However, mucosal immunity is related to the route of application of the antigen, the type of disease and the onset of the disease, and may have a dual role, especially in the development of autoimmune diseases. The mucosal application of antigens may aggravate the condition.