Brocke S, Hausmann S, Steinman L, Wucherpfennig K W
Neurological Diseases Section, NINDS, National Institutes of Health, Bethesda, MD 20892-1400, USA.
Semin Immunol. 1998 Feb;10(1):57-67. doi: 10.1006/smim.1997.0105.
The mechanisms by which microbial peptide antigens and superantigens might initiate and perpetuate autoimmune responses against antigens of the central nervous system are discussed. A model will be proposed that includes the initial activation of naive T lymphocytes through T cell receptor-mediated recognition of microbial antigens presented by MHC class II molecules. This event might be followed by re-activation of autoreactive T cells by bacterial and viral superantigens. Both mechanisms could lead to acute and relapsing autoimmune disease.
本文讨论了微生物肽抗原和超抗原引发并维持针对中枢神经系统抗原的自身免疫反应的机制。我们将提出一个模型,该模型包括通过T细胞受体介导识别由MHC II类分子呈递的微生物抗原,从而初始激活幼稚T淋巴细胞。此事件之后可能会发生细菌和病毒超抗原对自身反应性T细胞的再激活。这两种机制都可能导致急性和复发性自身免疫疾病。