B7 expression on thymic medullary epithelium correlates with epithelium-mediated deletion of V beta 5+ thymocytes.

摘要: Recent evidence suggests that I-E+ thymic epithelium, especially medullary can induce partial deletion of superantigen-reactive T cells expressing TcR V beta 5, 11, and 17. To seek further information on this issue, we constructed bone marrow chimeras in which MHC class II I-E is expressed epithelial at various levels locations; the were reconstituted with stem from 5 transgenic mice. Intrathymic was restricted to relatively mature (expressing high levels), degree correlated density expression medulla rather than cortex; selective epithelium caused prominent deletion. Interestingly, immunostaining normal chimeric mice revealed B7 (the ligand for CD28) largely a subset cells; these are co-express specific carbohydrate bound by lectin UEA-1. lower thymuses II-deficient (A b-/-) T-cell-deficient (SCID), suggesting up-regulated during CD4+ thymocyte selection. In support idea, thymus restored level SCID Because correlates costimulatory signal cells, related antigens may explain why play more role cortical epithelium.