Role of Interleukin 36γ in Host Defense Against Tuberculosis

Fadhil Ahsan, Pedro Moura-Alves, Ute Guhlich-Bornhof, Marion Klemm, Stefan H.E. Kaufmann, Jeroen Maertzdorf

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)


Tuberculosis remains a major killer worldwide, not the least because of our incomplete knowledge of protective and pathogenic immune mechanism. The roles of the interleukin 1 (IL-1) and interleukin 18 pathways in host defense are well established, as are their regulation through the inflammasome complex. In contrast, the regulation of interleukin 36γ (IL-36γ), a recently described member of the IL-1 family, and its immunological relevance in host defense remain largely unknown. Here we show that Mycobacterium tuberculosis infection of macrophages induces IL-36γ production in a 2-stage-regulated fashion. In the first stage, microbial ligands trigger host Toll-like receptor and MyD88-dependent pathways, leading to IL-36γ secretion. In the second stage, endogenous IL-1β and interleukin 18 further amplify IL-36γ synthesis. The relevance of this cytokine in the control of M. tuberculosis is demonstrated by IL-36γ-induced antimicrobial peptides and IL-36 receptor-dependent restriction of M. tuberculosis growth. Thus, we provide first insight into the induction and regulation of the proinflammatory cytokine IL-36γ during tuberculosis.

Original languageEnglish
Pages (from-to)464-474
Number of pages11
JournalJournal of Infectious Diseases
Issue number3
Publication statusPublished - 1 Aug 2016
Externally publishedYes


  • IL-36γ
  • Mycobacterium tuberculosis
  • TLR
  • antimicrobial peptide
  • inflammasome


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