期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 1, 页码 464-470出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002693
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资金
- Spanish Ministerio de Ciencia e Innovacion [BFU2009-06958, SAF2007-63622-C02, FIPSE 360783-09]
Monocytes and macrophages are targets of HIV-1 infection and play critical roles in multiple aspects of viral pathogenesis. During the differentiation of monocytes to macrophages, adhesion molecules such as integrins are upregulated; therefore, they provide signals that control the process and subsequently may render macrophages more susceptible to HIV-1 infection. Previous work demonstrated that blocking alpha(v)-containing integrins triggered a signal transduction pathway leading to the inhibition of NF-kappa B-dependent HIV-1 transcription. In this paper, we show the influence of the different alpha(v)-coupled beta integrins in HIV-1 replication in macrophages. Inhibition of beta integrins, either by specific mAbs, small arginine-glycine-aspartic acid (RGD) mimetic compounds, or RNA interference, showed that integrin beta(5) was the major contributor to the integrin-mediated blockade of HIV-1 replication. Importantly, such inhibition did not induce changes in cell adhesion to the substrate. In conclusion, our results reveal a significant role of the integrin dimmer alpha(v)beta(5) in HIV-1 infection of macrophages. The Journal of Immunology, 2011, 186: 464-470.
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