Chirmule N, Kalyanaraman V, Oyaizu N, Pahwa S
Department of Pediatrics, North Shore University Hospital, Cornell University Medical College, Manhasset, NY 11030.
J Acquir Immune Defic Syndr (1988). 1988;1(5):425-30.
Infection with the human immunodeficiency virus (HIV-1) leads to a wide range of immunological abnormalities. We have shown that native envelope glycoproteins (gp120) of HIV-1 inhibit antigen-specific and anti-CD3 induced lymphoproliferation of normal lymphocytes. We have demonstrated that gp120 binds to CD4 positive T lymphocytes and is internalized. These studies suggest that interaction of gp120 with the CD4 receptor may be sufficient to inhibit antigen-specific T cell responses that are mediated via the CD3-Ti receptor complex. Such an event could represent another mechanism by which the overall immune function of the CD4 positive T lymphocyte is depressed and may be relevant in planning investigations on the ongoing vaccine trial involving envelope glycoproteins.
感染人类免疫缺陷病毒（HIV-1）会导致多种免疫异常。我们已经表明，HIV-1的天然包膜糖蛋白（gp120）可抑制正常淋巴细胞的抗原特异性和抗CD3诱导的淋巴细胞增殖。我们已经证明gp120与CD4阳性T淋巴细胞结合并被内化。这些研究表明，gp120与CD4受体的相互作用可能足以抑制经由CD3-Ti受体复合物介导的抗原特异性T细胞反应。这样的事件可能代表了CD4阳性T淋巴细胞整体免疫功能被抑制的另一种机制，并且可能与正在进行的涉及包膜糖蛋白的疫苗试验的研究规划相关。
