Thalidomide-induced antigen-specific immune stimulation in patients with human immunodeficiency virus type 1 and tuberculosis

被引:50
作者
Bekker, LG
Haslett, P
Maartens, G
Steyn, L
Kaplan, G
机构
[1] Rockefeller Univ, Cellular Physiol & Immunol Lab, New York, NY 10021 USA
[2] Univ Cape Town, Dept Med, ZA-7925 Cape Town, South Africa
[3] Univ Cape Town, Dept Med Microbiol, ZA-7925 Cape Town, South Africa
关键词
D O I
10.1086/315328
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Thalidomide, which inhibits monocyte tumor necrosis factor (TNF)-alpha production and costimulates T cells, was tested for immune modulation in patients with human immunodeficiency virus (HIV) infection and tuberculosis (TB) in a placebo-controlled study. Thalidomide therapy resulted in increased levels of plasma interleukin (IL)-2 receptor, soluble CD8, interferon-gamma, and IL-12, indicating immune stimulation. TNF-alpha levels were not reduced. Thalidomide treatment increased CD4(+) and CD8(+) T cell counts and lymphocyte proliferation to purified protein derivative. Immune stimulation was not associated with an increase in plasma HIV levels. In vivo, a thalidomide dose-dependent costimulatory effect on T cell proliferation and HIV replication was observed after stimulation with antigens or antf-CD3, respectively Thalidomide-induced increased viral replication in CD4(+) T cells was abrogated by adding back autologous CD8(+) T cells. Thus, in the presence of thalidomide, antigen-specific immune responses in vitro and in patients with HTV/TB were enhanced.
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页码:954 / 965
页数:12
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