CC趋化因子增强HIV-1 T嗜性毒株在CD4(+) T细胞中的复制：信号转导的作用
CC-chemokines enhance the replication of T-tropic strains of HIV-1 in CD4(+) T cells: role of signal transduction.
作者信息
Kinter A, Catanzaro A, Monaco J, Ruiz M, Justement J, Moir S, Arthos J, Oliva A, Ehler L, Mizell S, Jackson R, Ostrowski M, Hoxie J, Offord R, Fauci A S
机构信息
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11880-5. doi: 10.1073/pnas.95.20.11880.
Abstract
This study demonstrates that several CC-chemokines, including those that inhibit entry and replication of macrophage-tropic strains of HIV, increase the replication of T cell (T)-tropic strains in CD4(+) T cells. Enhancement of T-tropic HIV replication is observed at early stages of replication, requires signaling through inhibitory guanine nucleotide-binding regulatory (Gi) proteins, and is associated with increased cell surface colocalization of CD4 and the T-tropic HIV coreceptor CXCR4. These findings may further our understanding of the factors that influence the replication and spread of T-tropic strains of HIV in vivo and suggest that the use of cell signaling CC-chemokines as therapeutic agents for the purpose of limiting HIV replication in vivo should be approached with caution.
摘要
本研究表明，几种CC趋化因子，包括那些抑制HIV巨噬细胞嗜性毒株进入和复制的趋化因子，可增加CD4(+)T细胞中T细胞嗜性毒株的复制。在复制早期即可观察到T嗜性HIV复制增强，这需要通过抑制性鸟嘌呤核苷酸结合调节（Gi）蛋白进行信号传导，并且与CD4和T嗜性HIV共受体CXCR4在细胞表面的共定位增加有关。这些发现可能会加深我们对影响HIV T嗜性毒株在体内复制和传播因素的理解，并表明将细胞信号CC趋化因子用作体内限制HIV复制的治疗药物时应谨慎行事。
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