免疫学
主要组织相容性复合体
人类白细胞抗原
自身免疫
CD8型
抗原
多发性硬化
自身免疫性疾病
人口
细胞毒性T细胞
银屑病
生物
抗体
医学
遗传学
体外
环境卫生
作者
Manuel A. Friese,Lars Fugger
摘要
Abstract Traditionally, autoimmune pathogeneses have been attributed to CD4 + T lymphocytes, as in multiple sclerosis (MS), rheumatoid arthritis, type 1 diabetes mellitus, and/or to B lymphocytes, as in myasthenia gravis and systemic lupus erythematosus. That is because their primary genetic associations are mostly with certain human leukocyte antigen class II alleles, whose gene products present antigens to CD4 + T cells. Because few autoimmune diseases show stronger associations with major histocompatibility complex class I alleles (ankylosing spondylitis, Behçet's disease, and psoriasis), CD8 + T cells, which interact with major histocompatibility complex class I molecules, have been largely ignored in autoimmunity research. However, a variety of findings has recently revived interest in this population, particularly in MS. First, it shows associations with major histocompatibility complex class I alleles. Second, its lesions show a predominance of CD8 + T cells. Third, these represent effectors that can directly damage central nervous system target cells. Furthermore, several clinical trials of monoclonal antibodies specifically against CD4 + T cells, or the polarizing cytokines on which they depend, have failed to show any therapeutic benefit in MS, unlike broader‐spectrum antibodies that deplete all T cells. Here, we review the evidence that CD8 + T cells play a role in MS pathogenesis. Ann Neurol 2009;66:132–141
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