Isoniazid induces apoptosis of activated CD4+ T cells: Implications for post-therapy tuberculosis reactivation and reinfection

Sultan Tousif, Dhiraj Kumar Singh, Shaheer Ahmad, Prashini Moodley, Maitree Bhattacharyya, Luc Van Kaer, Gobardhan Das

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

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 reinfection, suggesting therapy-related immune impairment. Here we show that Isoniazid (INH) treatment dramatically reduces Mycobacterium tuberculosis antigen-specific immune responses, induces apoptosis in activated CD4+ T cells, and renders treated animals vulnerable to TB reactivation and reinfection. Consequently, our findings suggest that TB treatment is associated with immune impairment.

Original languageEnglish (US)
Pages (from-to)30190-30195
Number of pages6
JournalJournal of Biological Chemistry
Volume289
Issue number44
DOIs
StatePublished - Oct 31 2014

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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