Human T-bet Governs Innate and Innate-like Adaptive IFN-γ Immunity against Mycobacteria
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), invar...
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| Published in: | Cell Vol. 183; no. 7; p. 1826 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
23.12.2020
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| Subjects: | |
| ISSN: | 1097-4172, 1097-4172 |
| Online Access: | Get more information |
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| Abstract | 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 T
1 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 T
1
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 T
1
cells unable to compensate for this deficit. |
|---|---|
| AbstractList | 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 T
1 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 T
1
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 T
1
cells unable to compensate for this deficit. 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.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. |
| Author | Ogishi, Masato Errami, Abderrahmane Kobor, Michael S Maclsaac, Julia L Di Santo, James P Oleaga-Quintas, Carmen Glimcher, Laurie H Rahman, Mahbuba Kerner, Gaspard Sallusto, Federica Husquin, Lucas T Marr, Nico Al Ali, Fatima Bustamante, Jacinta Bousfiha, Aziz Batteux, Fréderic Croft, Carys A Ailal, Fatima Bourgey, Mathieu Seeleuthner, Yoann Weisshaar, Marc Quintana-Murci, Lluis Ma, Cindy S Boisson-Dupuis, Stéphanie Gruber, Conor Zhang, Peng Jeljeli, Mohamed Worley, Lisa Langlais, David Doisne, Jean-Marc Rozenberg, Flore Rosain, Jérémie Roynard, Manon El Baghdadi, Jamila Tangye, Stuart G Latorre, Daniela Bogunovic, Dusan Pan-Hammarström, Qiang Shen, Yichao Carroll, Thomas Elarabi, Houda Markle, Janet Puel, Anne Jarrossay, David Benhsaien, Ibithal Abel, Laurent Casanova, Jean-Laurent Yang, Rui Gros, Philippe Mele, Federico Khan, Taushif Han, Jing |
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Electronic address: ryang@rockefeller.edu – sequence: 2 givenname: Federico surname: Mele fullname: Mele, Federico organization: Center of Medical Immunology, Institute for Research in Biomedicine, Faculty of Biomedical Sciences, University of Italian Switzerland (USI), 6500 Bellinzona, Switzerland – sequence: 3 givenname: Lisa surname: Worley fullname: Worley, Lisa organization: Garvan Institute of Medical Research, Darlinghurst 2010, NSW, Australia; St Vincent's Clinical School, Faculty of Medicine, UNSW Sydney, Darlinghurst 2010, NSW, Australia – sequence: 4 givenname: David surname: Langlais fullname: Langlais, David organization: Department of Human Genetics, Department of Microbiology and Immunology, McGill University, Montreal, QC H3A 0G1, Canada; McGill University Genome Center, McGill Research Centre on Complex Traits, Montreal, QC H3A 0G1, Canada – sequence: 5 givenname: Jérémie surname: Rosain fullname: Rosain, Jérémie organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Necker Hospital for Sick Children, 75015 Paris, France; 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Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Necker Hospital for Sick Children, 75015 Paris, France; University of Paris, Imagine Institute, 75015 Paris, France; Study Center for Primary Immunodeficiencies, Necker Children Hospital, AP-HP, 75015 Paris, France – sequence: 52 givenname: Jean-Laurent surname: Casanova fullname: Casanova, Jean-Laurent email: casanova@rockefeller.edu organization: St Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, Rockefeller University, New York, NY 10065, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Necker Hospital for Sick Children, 75015 Paris, France; University of Paris, Imagine Institute, 75015 Paris, France; Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children, AP-HP, 75015 Paris, France; Howard Hughes Medical Institute, New York, NY, USA. Electronic address: casanova@rockefeller.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33296702$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
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| DOI | 10.1016/j.cell.2020.10.046 |
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| Keywords | innate-like adaptive lymphocyte IFN-γ innate lymphocyte mycobacterium immunodeficiency inborn errors of immunity Mendelian susceptibility to mycobacterial disease T-bet |
| Language | English |
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| Snippet | Inborn errors of human interferon gamma (IFN-γ) immunity underlie mycobacterial disease. We report a patient with mycobacterial disease due to inherited... |
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| SubjectTerms | Adaptive Immunity Amino Acid Sequence Base Sequence Cell Lineage Child, Preschool Chromatin - metabolism CpG Islands - genetics Dendritic Cells - metabolism DNA Methylation - genetics Epigenesis, Genetic Female Homozygote Humans Immunity, Innate INDEL Mutation - genetics Infant Interferon-gamma - immunology Interferon-gamma - metabolism Killer Cells, Natural - cytology Killer Cells, Natural - metabolism Loss of Function Mutation - genetics Male Mycobacterium - immunology Mycobacterium Infections - genetics Mycobacterium Infections - immunology Mycobacterium Infections - microbiology Pedigree T-bet Transcription Factor T-Box Domain Proteins - chemistry T-Box Domain Proteins - deficiency T-Box Domain Proteins - genetics T-Box Domain Proteins - metabolism T-Lymphocytes, Helper-Inducer - immunology Transcriptome - genetics |
| Title | Human T-bet Governs Innate and Innate-like Adaptive IFN-γ Immunity against Mycobacteria |
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