Thalidomide‐Induced Antigen‐Specific Immune Stimulation in Patients with Human Immunodeficiency Virus Type 1 and Tuberculosis

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Abstract
Thalidomide, which inhibits monocyte tumor necrosis factor (TNF)-α 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-γ, and IL-12, indicating immune stimulation. TNF-α 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 anti-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 HIV/TB were enhanced.

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