免疫系统
重症肌无力
免疫学
淋巴因子
乙酰胆碱受体
生物
淋巴细胞
受体
生物化学
作者
Premkumar Christadoss,Jon Lindstrom,N Talal,C R Duvic,A Kalantri,Suchitra Shenoy
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:1986-09-15
卷期号:137 (6): 1845-1849
被引量:23
标识
DOI:10.4049/jimmunol.137.6.1845
摘要
The role of lymphokines secreted by acetylcholine receptor (AChR)-reactive lymphocytes in the regulation of an autoimmune response to AChR has not been studied in the human or murine model of myasthenia gravis. We investigated whether AChR-immune lymphocytes derived from mice with experimental autoimmune myasthenia gravis (EAMG) can produce an AChR-specific, genetically controlled soluble factor with biologic activity. AChR-reactive lymphocytes of mice with EAMG secreted an AChR-specific helper factor in vitro, which induced proliferation of AChR-immune but not Mycobacterium tuberculosis-immune lymphocytes. Recombinant, I-A mutant, and monoclonal anti-I-A antibody analyses suggest that AChR-specific helper factor-induced lymphocyte proliferation is controlled by an immune response gene at the I-A subregion of the murine major histocompatibility complex, and is mediated by the I-A molecule.
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