دورية أكاديمية
أعرض في EDS

Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells.

التفاصيل البيبلوغرافية
العنوان: Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells.
المؤلفون: Berkson JD; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.; Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195., Slichter CK; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.; Department of Global Health, University of Washington, Seattle, WA 98195., DeBerg HA; Systems Immunology Division, Benaroya Research Institute, Seattle, WA 98101., Delaney MA; Zoological Pathology Program, University of Illinois, Brookfield, IL 60513., Woodward-Davis AS; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109., Maurice NJ; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.; Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195., Lwo Y; Department of Periodontics, University of Washington, Seattle, WA 98195; and., Ko A; Department of Periodontics, University of Washington, Seattle, WA 98195; and., Hsu J; Department of Periodontics, University of Washington, Seattle, WA 98195; and., Chiu YW; Department of Periodontics, University of Washington, Seattle, WA 98195; and., Linsley PS; Systems Immunology Division, Benaroya Research Institute, Seattle, WA 98101., Dixon D; Department of Periodontics, University of Washington, Seattle, WA 98195; and., Prlic M; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109; mprlic@fhcrc.org.; Department of Global Health, University of Washington, Seattle, WA 98195.; Department of Immunology, University of Washington, Seattle, WA 98109.
المصدر: ImmunoHorizons [Immunohorizons] 2020 Jan 23; Vol. 4 (1), pp. 14-22. Date of Electronic Publication: 2020 Jan 23.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: American Association of Immunologists, Inc Country of Publication: United States NLM ID: 101708159 Publication Model: Electronic Cited Medium: Internet ISSN: 2573-7732 (Electronic) Linking ISSN: 25737732 NLM ISO Abbreviation: Immunohorizons Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Rockville, Maryland : American Association of Immunologists, Inc., [2017]-
مواضيع طبية MeSH: Antigens, Surface/*immunology , CD8-Positive T-Lymphocytes/*immunology , CTLA-4 Antigen/*immunology , Cytokines/*immunology , Mucosal-Associated Invariant T Cells/*immunology, Adolescent ; Adult ; Aged ; Aged, 80 and over ; Blood/immunology ; Female ; Gene Expression/immunology ; Humans ; Inflammation/genetics ; Male ; Middle Aged ; Mucous Membrane/immunology ; Receptors, Antigen, T-Cell/immunology
مستخلص: Mucosal-associated invariant T (MAIT) cells acquire effector function in response to proinflammatory signals, which synergize with TCR-mediated signals. We asked if cell-intrinsic regulatory mechanisms exist to curtail MAIT cell effector function akin to the activation-induced expression of inhibitory receptors by conventional T cells. We examined human MAIT cells from blood and oral mucosal tissues by RNA sequencing and found differential expression of immunoregulatory genes, including CTLA-4, by MAIT cells isolated from tissue. Using an ex vivo experimental setup, we demonstrate that inflammatory cytokines were sufficient to induce CTLA-4 expression on the MAIT cell surface in the absence of TCR signals. Even brief exposure to the cytokines IL-12, IL-15, and IL-18 was sufficient for sustained CTLA-4 expression by MAIT cells. These data suggest that control of CTLA-4 expression is fundamentally different between MAIT cells and conventional T cells. We propose that this mechanism serves to limit MAIT cell-mediated tissue damage.
(Copyright © 2020 The Authors.)
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معلومات مُعتمدة: T32 AI007509 United States AI NIAID NIH HHS; R01 AI123323 United States AI NIAID NIH HHS; R21 DE026565 United States DE NIDCR NIH HHS; T32 AI007140 United States AI NIAID NIH HHS; T32 GM007270 United States GM NIGMS NIH HHS; F99 CA245735 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Antigens, Surface)
0 (CTLA-4 Antigen)
0 (CTLA4 protein, human)
0 (Cytokines)
0 (Receptors, Antigen, T-Cell)
تواريخ الأحداث: Date Created: 20200125 Date Completed: 20200513 Latest Revision: 20200715
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC7357853
DOI: 10.4049/immunohorizons.1900061
PMID: 31974109
قاعدة البيانات: MEDLINE
الوصف
تدمد:2573-7732
DOI:10.4049/immunohorizons.1900061