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© Research
Publication : Cell

Human T-bet Governs Innate and Innate-like Adaptive IFN-γ Immunity against Mycobacteria.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell - 23 Dec 2020

Yang R, Mele F, Worley L, Langlais D, Rosain J, Benhsaien I, Elarabi H, Croft CA, Doisne JM, Zhang P, Weisshaar M, Jarrossay D, Latorre D, Shen Y, Han J, Ogishi M, Gruber C, Markle J, Al Ali F, Rahman M, Khan T, Seeleuthner Y, Kerner G, Husquin LT, Maclsaac JL, Jeljeli M, Errami A, Ailal F, Kobor MS, Oleaga-Quintas C, Roynard M, Bourgey M, El Baghdadi J, Boisson-Dupuis S, Puel A, Batteux F, Rozenberg F, Marr N, Pan-Hammarström Q, Bogunovic D, Quintana-Murci L, Carroll T, Ma CS, Abel L, Bousfiha A, Di Santo JP, Glimcher LH, Gros P, Tangye SG, Sallusto F, Bustamante J, Casanova JL,

Link to Pubmed [PMID] – 33296702

Link to DOI – S0092-8674(20)31453-710.1016/j.cell.2020.10.046

Cell 2020 Dec; 183(7): 1826-1847.e31

Inborn errors of human interferon gamma (IFN-γ) immunity underlie mycobacterial disease. We report a patient with mycobacterial disease due to inherited deficiency of the transcription factor T-bet. The patient has extremely low counts of circulating Mycobacterium-reactive natural killer (NK), invariant NKT (iNKT), mucosal-associated invariant T (MAIT), and Vδ2+ γδ T lymphocytes, and of Mycobacterium-non reactive classic TH1 lymphocytes, with the residual populations of these cells also producing abnormally small amounts of IFN-γ. Other lymphocyte subsets develop normally but produce low levels of IFN-γ, with the exception of CD8+ αβ T and non-classic CD4+ αβ TH1∗ lymphocytes, which produce IFN-γ normally in response to mycobacterial antigens. Human T-bet deficiency thus underlies mycobacterial disease by preventing the development of innate (NK) and innate-like adaptive lymphocytes (iNKT, MAIT, and Vδ2+ γδ T cells) and IFN-γ production by them, with mycobacterium-specific, IFN-γ-producing, purely adaptive CD8+ αβ T, and CD4+ αβ TH1∗ cells unable to compensate for this deficit.

https://pubmed.ncbi.nlm.nih.gov/33296702