The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Regulation of type 17 helper T-cell function by nitric oxide during inflammation
Open accessAbstract
Type 17 helper T (Th17) cells are implicated in the pathogenesis many of human autoimmune diseases. Development of Th17 can be enhanced by the activation of aryl hydrocarbon receptor (AHR) whose ligands include the environmental pollutant dioxin, potentially linking environmental factors to the increased prevalence of autoimmune disease. We report here that nitric oxide (NO) can suppress the proliferation and function of polarized murine and human Th17 cells. NO also inhibits AHR expression in Th17 cells and the downstream events of AHR activation, including IL-22, IL-23 receptor, and Cyp1a1. Conversely, NO did not affect the polarization of Th17 cells from mice deficient in AHR. Furthermore, mice lacking inducible nitric oxide synthase ( Nos2 −/− ) developed more severe experimental autoimmune encephalomyelitis than WT mice, with elevated AHR expression, increased IL-17A, and IL-22 synthesis. NO may therefore represent an important endogenous regulator to prevent overexpansion of Th17 cells and control of autoimmune diseases caused by environmental pollutants.
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“Increased iNOS expression in T cells also regulates Th17 cell differentiation [114].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [114]
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Metadata
- Authors
- Niedbala, W., Alves-Filho, J. C., Fukada, S. Y., Vieira, S. M., Mitani, A., Sonego, F., Mirchandani, A., Nascimento, D. C., Cunha, F. Q., & Liew, F. Y.
- Affiliations
- Institute of Infection, Immunity, and Inflammation, University of Glasgow, Glasgow G12 8TA, Scotland;
- Universidade de São Paulo (BR)
- Aichi Gakuin University (JP)
- University of Glasgow (GB)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2011-05-16
- Volume
- 108
- Issue
- 22
- Pages
- 9220-9225
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3107290
- OpenAlex
- W1997158650
- Cited by
- 117
- References
- 45
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 6 · 2023: 7 · 2022: 13 · 2021: 6 · 2020: 5 · 2019: 11 · 2018: 9 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 8 · 2013: 14 · 2012: 8
- FWCI
- 4.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Scientific Electronic Library Online (São Paulo Research Foundation, Latin American and Caribbean Center on Health Sciences Information, Conselho Nacional de Desenvolvimento Científico e Tecnológico) (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- Th17 cells, nitric oxide, aryl hydrocarbon receptor, dioxins, inducible nitric oxide synthase, experimental autoimmune encephalomyelitis, IL-22, IL23R, CYP1A1, IL-17A, autoimmune disease, inflammation, environmental pollutants
- MeSH terms
- Interleukin-22, Animals, Autoimmune Diseases, Cyclic GMP, T-Lymphocytes, Helper-Inducer, Humans, Inflammation, Interleukin-2, Interleukins, Ligands, Mice, Inbred BALB C, Models, Biological, Nitric Oxide, Interleukin-10, Receptors, Interleukin, Cytochrome P-450 CYP1A1, Cell Proliferation, Proto-Oncogene Protein c-ets-1, Mice, Nitric Oxide Synthase Type II, Th17 Cells
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