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A mechanism of resistance to HIV-1 entry: inefficient interactions of CXCR4 with CD4 and gp120 in macrophages.

机译:抵抗HIV-1进入的机制:巨噬细胞中CXCR4与CD4和gp120的无效相互作用。

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摘要

To test the hypothesis that inefficient interactions of CXCR4 with CD4 and gp120 could affect HIV-1 entry, we incubated macrophages, monocytes, and lymphocytes with gp120 and coimmunoprecipitated CD4 by using anti-CXCR4 antibodies. CD4 was efficiently coimmunoprecipitated in lymphocytes and monocytes but not in macrophages. Overexpression of CD4 in macrophages resulted in detection of CD4-CXCR4 and gp120-CD4-CXCR4 complexes in parallel with the restoration of macrophage fusion susceptibility. These results suggest a mechanism of resistance to entry of some X4 HIV-1 strains into macrophages and a method for dissection of the initial stages of HIV entry.
机译:为了检验CXCR4与CD4和gp120的无效相互作用可能影响HIV-1进入的假说,我们使用抗CXCR4抗体将巨噬细胞,单核细胞和淋巴细胞与gp120和共免疫沉淀的CD4孵育。 CD4在淋巴细胞和单核细胞中有效共免疫沉淀,而在巨噬细胞中则不能。 CD4在巨噬细胞中的过表达导致CD4-CXCR4和gp120-CD4-CXCR4复合物的检测,同时恢复巨噬细胞融合敏感性。这些结果表明对某些X4 HIV-1菌株进入巨噬细胞具有抗性的机制,以及解剖HIV进入初期的方法。

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