Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis.
Animals
Biomarkers
Cytokines
/ genetics
Female
Histocompatibility Antigens Class I
/ genetics
Humans
Immunity, Innate
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
Minor Histocompatibility Antigens
/ genetics
Mucosal-Associated Invariant T Cells
/ physiology
RNA, Messenger
/ genetics
Sepsis
/ immunology
MAIT cells
human
immunology
inflammation
innate-like T cell
medicine
mouse
sepsis
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
09 11 2020
09 11 2020
Historique:
received:
30
01
2020
accepted:
09
11
2020
pubmed:
10
11
2020
medline:
16
3
2021
entrez:
9
11
2020
Statut:
epublish
Résumé
Sepsis is a systemic inflammatory response to infection and a leading cause of death. Mucosal-associated invariant T (MAIT) cells are innate-like T cells enriched in mucosal tissues that recognize bacterial ligands. We investigated MAIT cells during clinical and experimental sepsis, and their contribution to host responses. In experimental sepsis, MAIT-deficient mice had significantly increased mortality and bacterial load, and reduced tissue-specific cytokine responses. MAIT cells of WT mice expressed lower levels of IFN-γ and IL-17a during sepsis compared to sham surgery, changes not seen in non-MAIT T cells. MAIT cells of patients at sepsis presentation were significantly reduced in frequency compared to healthy donors, and were more activated, with decreased IFN-γ production, compared to both healthy donors and paired 90-day samples. Our data suggest that MAIT cells are highly activated and become dysfunctional during clinical sepsis, and contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.
Identifiants
pubmed: 33164745
doi: 10.7554/eLife.55615
pii: 55615
pmc: PMC7679140
doi:
pii:
Substances chimiques
Biomarkers
0
Cytokines
0
Histocompatibility Antigens Class I
0
Minor Histocompatibility Antigens
0
Mr1 protein, mouse
0
RNA, Messenger
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAID NIH HHS
ID : R01 AI130378
Pays : United States
Organisme : NIA NIH HHS
ID : R03 AG040631
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002538
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL092161
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM134331
Pays : United States
Organisme : NHGRI NIH HHS
ID : T32 HG008962
Pays : United States
Organisme : NCATS NIH HHS
ID : TL1 TR002540
Pays : United States
Organisme : CSRD VA
ID : I01 CX001696
Pays : United States
Organisme : NIA NIH HHS
ID : K01 AG059892
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG048022
Pays : United States
Informations de copyright
© 2020, Trivedi et al.
Déclaration de conflit d'intérêts
ST, DL, CA, CA, AB, EM, OJ, AT, MM, RC, JH, MR, DL No competing interests declared
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