Isoniazid induces apoptosis of activated CD4+ T cells: implications for post-therapy tuberculosis reactivation and re-infection [Microbiology]

September 8th, 2014 by Tousif, S., Singh, D. K., Ahmad, S., Moodley, P., Bhattacharyya, M., Kaer, L. V., Das, G.

Tuberculosis (TB) remains the second highest killer from a single infectious disease worldwide. Current therapy of TB is lengthy and consists of multiple expensive antibiotics, in a strategy referred to as Directly Observed Treatment, Short-Course (DOTS). Although this therapy is effective, it has serious disadvantages. These therapeutic agents are toxic and are associated with the development of a variety of drug-resistant TB strains. Furthermore, patients treated with DOTS exhibit enhanced post-treatment susceptibility to TB reactivation and re-infection, suggesting therapy-related immune impairment. Here we show that isoniazid (INH) treatment dramatically reduces M.tb antigen-specific immune responses, induces apoptosis in activated CD4+ T cells, and renders treated animals vulnerable to TB reactivation and re-infection. Consequently, our findings suggest that TB treatment is associated with immune impairment.
  • Posted in Journal of Biological Chemistry, Publications
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