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Yang, Rui; Mele, Federico; Worley, Lisa; Langlais, David; Rosain, Jérémie; Benhsaien, Ibithal; Elarabi, Houda; Croft, Carys A.; Doisne, Jean-Marc; Zhang, Peng; Weisshaar, Marc; Jarrossay, David; Latorre, Daniela; Shen, Yichao; Han, Jing; Ogishi, Masato; Gruber, Conor; Markle, Janet; Al Ali, Fatima; Rahman, Mahbuba; Khan, Taushif; Seeleuthner, Yoann; Kerner, Gaspard; Husquin, Lucas T.; Maclsaac, Julia L.; Jeljeli, Mohamed; Errami, Abderrahmane; Ailal, Fatima; Kobor, Michael S.; Oleaga-Quintas, Carmen; Roynard, Manon; Bourgey, Mathieu; El Baghdadi, Jamila; Boisson-Dupuis, Stéphanie; Puel, Anne; Batteux, Fréderic; Rozenberg, Flore; Marr, Nico; Pan-Hammarström, Qiang; Bogunovic, Dusan; Quintana-Murci, Lluis; Carroll, Thomas; Ma, Cindy S.; Abel, Laurent; Bousfiha, Aziz; Di Santo, James P.; Glimcher, Laurie H.; Gros, Philippe; Tangye, Stuart G.; Sallusto, Federica; Bustamante, Jacinta; Casanova, Jean-Laurent
Cell, 12/2020, Letnik: 183, Številka: 7Journal Article
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. Display omitted •Human inherited T-bet deficiency underlies severe mycobacterial disease•The development of a variety of IFN-γ-producing lymphocyte subsets is impaired•The production of IFN-γ by innate and innate-like lymphocytes is impaired•Mycobacterium-specific αβ CD4 TH1∗ and CD8 cells produce IFN-γ normally Human T-bet is involved in the regulation of distinct leukocyte subsets, when compared with its mouse counterpart, with its deficiency underlying severe mycobacterial disease
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