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首页> 外文期刊>AIDS Research and Human Retroviruses >Interferon-gamma receptors in HIV-1 infection.
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Interferon-gamma receptors in HIV-1 infection.

机译:HIV-1感染中的γ-干扰素受体。

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We studied in vitro production of interferon-gamma and expression of interferon-gamma receptors (R1 and R2) by the peripheral blood mononuclear cells of 24 HIV-1-infected patients and 12 healthy volunteers. Interferon-gamma production was lower in HIV-1-infected patients compared with healthy volunteers (p < 0.05), and it further declined in patients with lower CD4+ T-cell counts. In contrast, expression of interferon-gamma R1 by CD4+ T lymphocytes was higher in HIV-infected patients than healthy volunteers (25% versus 10%, p < 0.05). In the HIV-infected group, interferon-gamma R1 expression increased with a decline in CD4+ T-cell count (r = -0.64, p < 0.001). Interferon-gamma R2 expression directly correlated with interferon-gamma R1 expression (p < 0.001). When stimulated with heat-killed Mycobacterium avium complex (MAC) and phorbol myristic acetate (PMA), the mononuclear cells of patients with advanced HIV-1 infection had lowered ability to produce additional interferon-gamma (either MAC or PMA) and interferon-gamma receptors (MAC). In conclusion, with progression of HIV-1 infection, interferon-gamma production declines whereas expression of interferon-gamma receptors (R1 and R2) increases. Persistent upregulation of both interferon-gamma R1 and R2 receptors probably favors development of type 2 T-helper cells environment and promotes viral replication. This dysfunction in the interferon-gamma pathway contributes to a further impairment in cellular immune function in patients with advanced HIV-1 infection, which may further increase susceptibility to opportunistic infections.
机译:我们研究了24名HIV-1感染患者和12名健康志愿者的外周血单核细胞的干扰素-γ的体外生产和干扰素-γ受体(R1和R2)的表达。与健康志愿者相比,HIV-1感染患者的干扰素-γ生成量较低(p <0.05),而CD4 + T细胞计数较低的患者其干扰素-γ生成量进一步下降。相反,HIV感染患者中CD4 + T淋巴细胞的干扰素-γR1表达高于健康志愿者(25%对10%,p <0.05)。在HIV感染组中,干扰素-γR1表达随着CD4 + T细胞计数的下降而增加(r = -0.64,p <0.001)。干扰素-γR2的表达与干扰素-γR1的表达直接相关(p <0.001)。当用热灭活的鸟分枝杆菌复合物(MAC)和佛波肉豆蔻乙酸酯(PMA)刺激时,晚期HIV-1感染患者的单核细胞产生其他干扰素-γ(MAC或PMA)和干扰素-γ的能力降低。受体(MAC)。总之,随着HIV-1感染的进展,干扰素-γ的产生下降,而干扰素-γ受体(R1和R2)的表达增加。干扰素-γR1和R2受体的持续上调可能有利于2型T辅助细胞环境的发展并促进病毒复制。干扰素-γ途径的这种功能障碍进一步加剧了晚期HIV-1感染患者的细胞免疫功能,从而可能进一步增加对机会性感染的敏感性。

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