دورية أكاديمية
أعرض في EDS

NLRC4 inhibits NLRP3 inflammasome and abrogates effective antifungal CD8 + T cell responses.

التفاصيل البيبلوغرافية
العنوان: NLRC4 inhibits NLRP3 inflammasome and abrogates effective antifungal CD8 + T cell responses.
المؤلفون: Souza COS; Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil., Ketelut-Carneiro N; Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.; Program in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA., Milanezi CM; Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil., Faccioli LH; Department of Clinical Analyses, Toxicology and Bromatological Science, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil., Gardinassi LG; Department of Biosciences and Technology, Institute of Tropical Pathology and Public Health, Federal University of Goiás, Goiânia, GO, Brazil., Silva JS; Department of Biochemistry and Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.; Fiocruz-Bi-Institutional Translational Medicine Platform, Ribeirão Preto, SP, Brazil.
المصدر: IScience [iScience] 2021 May 18; Vol. 24 (6), pp. 102548. Date of Electronic Publication: 2021 May 18 (Print Publication: 2021).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2018]-
مستخلص: The recognition of fungi by intracellular NOD-like receptors (NLRs) induces inflammasome assembly and activation. Although the NLRC4 inflammasome has been extensively studied in bacterial infections, its role during fungal infections is unclear. Paracoccidioidomycosis (PCM) is a pathogenic fungal disease caused by Paracoccidioides brasiliensis . Here, we show that NLRC4 confers susceptibility to experimental PCM by regulating NLRP3-dependent cytokine production and thus protective effector mechanisms. Early after infection, NLRC4 suppresses prostaglandin E 2 production, and consequently reduces interleukin (IL)-1β release by macrophages and dendritic cells in the lungs. IL-1β is required to control fungal replication via induction of the nitric oxide synthase 2 (NOS2) pathway. At a later stage of the disease, NLRC4 impacts IL-18 release, dampening robust CD8 + IFN-γ + T cell responses and enhancing mortality of mice. These findings demonstrate that NLRC4 promotes disease by regulating the production of inflammatory cytokines and cellular responses that depend on the NLRP3 inflammasome activity.
Competing Interests: The authors declare no competing interests.
(© 2021 The Authors.)
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فهرسة مساهمة: Keywords: Immunology; Mycology
تواريخ الأحداث: Date Created: 20210618 Latest Revision: 20210619
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8184506
DOI: 10.1016/j.isci.2021.102548
PMID: 34142053
قاعدة البيانات: MEDLINE
الوصف
تدمد:2589-0042
DOI:10.1016/j.isci.2021.102548