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内源性Toll样受体配体与自身免疫

Endogenous TLR ligands and autoimmunity.

作者信息

Wagner Hermann

机构信息

Institute of Medical Microbiology, Immunology and Hygiene, 81675 Munich, Germany.

出版信息

Adv Immunol. 2006;91:159-73. doi: 10.1016/S0065-2776(06)91004-9.

Abstract

Based on an evolutionary conserved repertoire Toll-like-receptors (TLRs) donate specificity to innate immune cells. Therefore, TLRs are considered as paradigmatic for "self" versus "non-self" discrimination. This view, however, needs to be modified since TLR's also appear to recognise "endogeneous", that is host-derived ligands, examples being host-derived DNA and -RNA. Here I discuss physiological and pathophysiological consequences of endogeneous ligand-recognition by TLRs. I conclude that endogeneous ligand recognition by TLRs drives sterile inflammation sustained by innate immune cells in certain autoimmune disorders.

摘要

基于进化保守的模式识别受体库,Toll样受体(TLRs)赋予先天免疫细胞特异性。因此,TLRs被视为区分“自身”与“非自身”的典范。然而,这种观点需要修正,因为TLRs似乎也能识别“内源性”,即宿主来源的配体,例如宿主来源的DNA和RNA。在此,我将讨论TLRs识别内源性配体的生理和病理生理后果。我的结论是,在某些自身免疫性疾病中,TLRs识别内源性配体可引发由先天免疫细胞维持的无菌性炎症。

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