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负选择、表位模拟与自身免疫。

Negative selection, epitope mimicry and autoimmunity.

机构信息

Department of Pathology, Brigham and Women's Hospital/Harvard Medical School, New Research Building 630 OB, 77 Avenue Louis Pasteur, Boston, MA 02115, United States.

出版信息

Curr Opin Immunol. 2017 Dec;49:51-55. doi: 10.1016/j.coi.2017.08.014. Epub 2017 Nov 3.

DOI:10.1016/j.coi.2017.08.014
PMID:29102863
Abstract

Infections often precede the onset of autoimmune disease and molecular (or epitope) mimicry is a plausible link. Cross-reacting epitopes are common between an infecting microorganism and the host because negative selection of self-reactive T-cells and B-cells is frequently incomplete. Complete eradication could lead to major voids in the immunologic repertoire. The association of an autoimmune disease with a microbial epitope may signify a causal relationship with the organism, an indirect connection through bystander effects, persistent infection or coincidence. There are well-established examples of a microbial mimic inducing a defined model of autoimmune disease in experimental animals but such instances are still relatively rare in humans. Establishing epitope mimicry as a direct cause opens opportunities for preventing the disease. Current approaches to cancer immunotherapy provides new examples of epitope mimicry between cancer antigens and normal tissue antigens.

摘要

感染通常先于自身免疫性疾病的发作,而分子(或表位)模拟是一种合理的联系。由于自身反应性 T 细胞和 B 细胞的阴性选择常常不完全,感染微生物和宿主之间存在常见的交叉反应表位。完全消除可能导致免疫谱中的重大空白。自身免疫性疾病与微生物表位的关联可能表明与该生物体存在因果关系,也可能是通过旁观者效应、持续感染或巧合的间接联系。有大量微生物模拟物在实验动物中诱导明确的自身免疫性疾病模型的例子,但在人类中这种情况仍然相对较少。将表位模拟确立为直接原因,为预防疾病提供了机会。当前的癌症免疫疗法方法为癌症抗原和正常组织抗原之间的表位模拟提供了新的范例。

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