Komanduri K V, Salha M D, Sékaly R P, McCune J M
Gladstone Institute of Virology and Immunology, San Francisco, CA 94141, USA.
J Immunol. 1997 Jan 15;158(2):544-9.
Infection by HIV-1 has been associated with perturbations in the TCR V beta repertoire, suggesting the involvement of a superantigen. Among the hallmarks of superantigens is the capacity to delete T cells bearing specific TCR V beta families in the developing thymus. To verify the presence of a superantigen in HIV-1, we analyzed the SCID-hu Thy/Liv TCR V beta repertoire within CD4+CD8+, CD4+CD8-, or CD4-CD8+ thymocytes subsets by flow cytometry using a panel of Abs recognizing about 60% of the TCR repertoire following injection of SEB or infection by two different HIV-1 isolates. Seven days following SEB injection, thymocyte subsets bearing TCR V beta 3, V beta 12, V beta 17, and V beta 20, but not V beta 5 or V beta 8 , were deleted relative to mock-injected mice. In contrast, no changes were observed in the TCR V beta repertoire in CD4+CD8+, CD4+CD8-, or CD4-CD8+ thymocyte subsets after infection with HIV-1. The T cell depletion caused by HIV-1 infection is most likely not mediated by an HIV-encoded superantigen.
HIV-1感染与TCR Vβ库的紊乱有关,提示有超抗原参与。超抗原的特征之一是能够在发育中的胸腺中清除携带特定TCR Vβ家族的T细胞。为了验证HIV-1中是否存在超抗原,我们在注射SEB或感染两种不同的HIV-1分离株后,通过流式细胞术使用一组识别约60%TCR库的抗体,分析了SCID-hu Thy/Liv TCR Vβ库在CD4+CD8+、CD4+CD8-或CD4-CD8+胸腺细胞亚群中的情况。注射SEB七天后,相对于模拟注射的小鼠,携带TCR Vβ3、Vβ12、Vβ17和Vβ20但不携带Vβ5或Vβ8的胸腺细胞亚群被清除。相比之下,感染HIV-1后,CD4+CD8+、CD4+CD8-或CD4-CD8+胸腺细胞亚群中的TCR Vβ库未观察到变化。HIV-1感染导致的T细胞耗竭很可能不是由HIV编码的超抗原介导的。