Pedroza-Martins Livia, Boscardin W John, Anisman-Posner Deborah J, Redsar Beverly N, Bryson Yvonne J, Yang Otto O, Uittenbogaart Christel H
Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, California 90095-1747, USA.
AIDS. 2006 Apr 4;20(6):939-42. doi: 10.1097/01.aids.0000218563.12897.ba.
As interferon-gamma (IFN-gamma) is produced at lower levels by neonatal than adult T cells, we determined whether IFN-gamma influences HIV-1 replication in thymocytes. IFN-gamma significantly decreased replication of R5 but not X4 viruses, and reduced depletion of CD3(hi)CD27 (mature) thymocytes, the preferential targets for R5 HIV-1. Thus infection and depletion of functionally mature thymocytes that can produce endogenous IFN-gamma may mutually contribute to HIV-1 replication in the thymus and to reduced T-cell output.
由于新生儿T细胞产生的干扰素-γ(IFN-γ)水平低于成人T细胞,我们研究了IFN-γ是否影响胸腺细胞中的HIV-1复制。IFN-γ显著降低了R5病毒而非X4病毒的复制,并减少了R5 HIV-1的优先靶标CD3(hi)CD27(成熟)胸腺细胞的耗竭。因此,能够产生内源性IFN-γ的功能成熟胸腺细胞的感染和耗竭可能共同促进HIV-1在胸腺中的复制以及T细胞输出的减少。