作者: Hye-Jung Kim , Bert Verbinnen , Xiaolei Tang , Linrong Lu , Harvey Cantor
DOI: 10.1038/NATURE09370
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摘要: Analysis of the immune system has defined a subset CD4+ T cells, termed Treg, that can inhibit excessive inflammatory responses. However, no cells genetically programmed to autoantibody formation and systemic-lupus-erythematosus-like disease have so far been defined. A mechanism fitting description now identified in mice. CD8+ (CD8+ Treg) is shown prevent maintain self-tolerance process involves recognition Qa-1 peptide ligands expressed at surface follicular helper cells. detailed understanding this aspect immune-system regulation could lead new approaches for treatment systemic lupus erythematosus other autoimmune disorders. Immune recognize 'self' tissues need be eliminated or controlled order diseases. Here, T-cell population delineated necessary self tolerance Genetic disruption inhibitory interaction between these their target Qa-1+ T-helper results lethal disease. The ability produce vigorous responses spare organs depends on elimination autoreactive B purging immature mature self-reactive incomplete may also require involvement suppress responses1. Regulatory (Treg) belonging role preventing untoward responses, but subsets development not yet defined2. Here we delineate regulatory lineage essential maintenance prevention murine These findings define sublineage CD8 rather than activate immunity represents an element response guarantor tolerance.