Nature Communications (Nov 2022)
Symbiotic bacteria-dependent expansion of MR1-reactive T cells causes autoimmunity in the absence of Bcl11b
- Kensuke Shibata,
- Chihiro Motozono,
- Masamichi Nagae,
- Takashi Shimizu,
- Eri Ishikawa,
- Daisuke Motooka,
- Daisuke Okuzaki,
- Yoshihiro Izumi,
- Masatomo Takahashi,
- Nao Fujimori,
- James B. Wing,
- Takahide Hayano,
- Yoshiyuki Asai,
- Takeshi Bamba,
- Yoshihiro Ogawa,
- Makoto Furutani-Seiki,
- Mutsunori Shirai,
- Sho Yamasaki
Affiliations
- Kensuke Shibata
- Department of Microbiology and Immunology, Graduate School of Medicine, Yamaguchi University
- Chihiro Motozono
- Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
- Masamichi Nagae
- Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
- Takashi Shimizu
- Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
- Eri Ishikawa
- Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
- Daisuke Motooka
- Department of Infection Metagenomics, Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University
- Daisuke Okuzaki
- Single Cell Genomics, Human Immunology, World Premier International Research Center Initiative Immunology Frontier Research Center, Osaka University
- Yoshihiro Izumi
- Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University
- Masatomo Takahashi
- Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University
- Nao Fujimori
- Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University
- James B. Wing
- Laboratory of Human Immunology (Single Cell Immunology), World Premier International Immunology Frontier Research Center, Osaka University
- Takahide Hayano
- Department of Systems Bioinformatics, Graduate School of Medicine, Yamaguchi University
- Yoshiyuki Asai
- Department of Systems Bioinformatics, Graduate School of Medicine, Yamaguchi University
- Takeshi Bamba
- Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University
- Yoshihiro Ogawa
- Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University
- Makoto Furutani-Seiki
- Systems Biochemistry in Pathology and Regeneration, Graduate School of Medicine, Yamaguchi University
- Mutsunori Shirai
- Department of Microbiology and Immunology, Graduate School of Medicine, Yamaguchi University
- Sho Yamasaki
- Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University
- DOI
- https://doi.org/10.1038/s41467-022-34802-8
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 15
Abstract
MR1 functions as an antigen presenting protein on cells in addition to MAIT cells. Here the authors use an early T cell-specific Bcl11b-deficient mouse that develops autoimmunity through a population of nonconventional MR1-restricted T cells and characterise their function.
