DECREASED ACCESSORY CELL-FUNCTION OF MACROPHAGES AFTER INFECTION WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INVITRO

被引:42
作者
ENNEN, J
SEIPP, I
NORLEY, SG
KURTH, R
机构
[1] Paul-Ehrlich-Institute, Langen
关键词
D O I
10.1002/eji.1830201114
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Peripheral blood monocytes from human immunodeficiency virus (HIV)‐infected individuals or AIDS‐related complex/AIDS patients ex vivo exhibit distinct alterations in some but not all immune functions. In studies presented here, monocytes from healthy donors were infected with HIV 1 in vitro and co‐cultures with autologous uninfected T lymphocytes were set up. The monocyte/macrophage (MΦ)‐dependent T cell function was determined by measurement of proliferative and secretory [interleukin (IL)2, interferon‐γ] responses to lectin (phytohemagglutinin), mitogen (anti‐CD3 monoclonal antibody), or recall antigen (tetanus toxoid, tuberculin). Accessory function of MΦ was normal after HIV infection when optimal amounts (10%–20%) were added to the T lymphocytes. However, HIV infection of MΦ significantly decreased T cell proliferative responses and secretion of IL 2 when supplemented at limited dilution (0.5%‐5%), although interferon‐γ production was not affected. Whereas the lipopolysaccharide‐triggered MΦ production of IL 1 was not impaired by HIV 1 infection, there was a significant decrease in this response when anti‐CD3 monoclonal antibody or tetanus toxoid were used to trigger the peripheral blood mononuclear cells. The impairment of proliferation of T lymphocytes in the presence of HIV 1‐infected MΦ could be overcome by addition of exogenous IL 1. Taken together, these data clearly show that the mononuclear phagocytedependent enhancement of stimulated T cell proliferation and lymphokine secretion is decreased when the restricted numbers of monocytes/MΦ are HIV 1 infected. There are, therefore, two possible roles of MΦ in HIV infection and progression to disease. First, as a reservoir and vehicle for dissemination of the virus, and second, as an immune cell whose essential functions are impaired by infection. Copyright © 1990 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
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页码:2451 / 2456
页数:6
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