Smith P D, Meng G, Sellers M T, Rogers T S, Shaw G M
Department of Medicine (Gastroenterology), University of Alabama at Birmingham, 35294, USA.
J Leukoc Biol. 2000 Sep;68(3):360-5.
Mucosal surfaces are the portal of entry for most HIV-1 infections and play an important role in disease pathogenesis. To characterize the biological parameters of HIV-1 infection in mucosal cells, we used purified lamina propria lymphocytes and macrophages from normal human small intestine to determine the distribution of the HIV-1 receptor and coreceptors on intestinal mononuclear cells and the permissiveness of these cells to HIV-1 infection. Lamina propria lymphocytes expressed CD4, CCR5, and CXCR4. In contrast, lamina propria macrophages expressed CD4 but not CCR5 or CXCR4. Intestinal lymphocytes supported replication by R5 and X4 isolates of HIV-1, but lamina propria macrophages were permissive to neither. RANTES, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta inhibited infection of intestinal lymphocytes by BaL, indicating that R5 infection of the intestinal lymphocytes was mediated by CCR5. Thus, resident lamina propria lymphocytes, not macrophages, are the target mononuclear cell for HIV-1 infection in the intestinal mucosa during early HIV-1 infection.
黏膜表面是大多数HIV-1感染的进入门户，在疾病发病机制中起重要作用。为了表征HIV-1在黏膜细胞中感染的生物学参数，我们使用从正常人小肠中纯化的固有层淋巴细胞和巨噬细胞来确定HIV-1受体和共受体在肠道单核细胞上的分布以及这些细胞对HIV-1感染的易感性。固有层淋巴细胞表达CD4、CCR5和CXCR4。相比之下，固有层巨噬细胞表达CD4，但不表达CCR5或CXCR4。肠道淋巴细胞支持HIV-1的R5和X4分离株的复制，但固有层巨噬细胞对两者均无易感性。RANTES、巨噬细胞炎性蛋白-1α（MIP-1α）和MIP-1β抑制BaL对肠道淋巴细胞的感染，表明肠道淋巴细胞的R5感染是由CCR5介导的。因此，在HIV-1感染早期，固有层常驻淋巴细胞而非巨噬细胞是肠道黏膜中HIV-1感染的靶单核细胞。
