Tumor Necrosis Factor–α Increased Production during Thalidomide Treatment in Patients with Tuberculosis and Human Immunodeficiency Virus Coinfection

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Abstract
We read with interest the article by Bekker et al. [1] on the role of thalidomide-induced antigen-specific immune stimulation in patients with human immunodeficiency virus (HIV) and Mycobacterium tuberculosis coinfection. In their report, it is suggested that thalidomide treatment of HIV-infected patients does not reduce plasma tumor necrosis factor (TNF)-α levels. The observation is explained by a differential effect of thalidomide on monocyte and T cell TNF-α production. In particular, the authors report that thalidomide inhibited TNF-α production by lipopolysaccharide-stimulated monocytes but failed to inhibit TNF-α production by activated T cells [2–5]. Finally, the authors found an increase in TNF-α production at day 21 of therapy in the thalidomidegroup, thus suggesting that the drug could be responsible for this increase by stimulation of T cell activation.

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