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      Th17/Treg Imbalance and Atherosclerosis

      review-article
      Author(s): 1 , 1 , 2 ,
      Publication date (Electronic):
      Journal: Disease Markers
      Publisher: Hindawi

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          Abstract

          Atherosclerosis is nowadays recognized as a chronic inflammatory disease of large arteries. In recent years, cellular and molecular biology studies on atherosclerosis confirmed that the occurrence and development are related to inflammation and autoimmunity. A variety of immune cells, cytokines, and transcription factors are involved in this process. Current studies found that T helper cell 17, regulatory T cells, and their cytokines play an important role in the development of atherosclerosis and vulnerable plaque rupture. Here, we provide a review of the up-to-date applications of T helper cell 17, regulatory T cells, cytokines, and their balance in the prognosis and therapy of atherosclerosis.

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          A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17.

          Heon Park, Zhaoxia Li, Xuexian O. Yang … (2005)
          Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-gamma negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
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            Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.

            Estelle Bettelli, Yijun Carrier, Wenda Gao … (2006)
            On activation, T cells undergo distinct developmental pathways, attaining specialized properties and effector functions. T-helper (T(H)) cells are traditionally thought to differentiate into T(H)1 and T(H)2 cell subsets. T(H)1 cells are necessary to clear intracellular pathogens and T(H)2 cells are important for clearing extracellular organisms. Recently, a subset of interleukin (IL)-17-producing T (T(H)17) cells distinct from T(H)1 or T(H)2 cells has been described and shown to have a crucial role in the induction of autoimmune tissue injury. In contrast, CD4+CD25+Foxp3+ regulatory T (T(reg)) cells inhibit autoimmunity and protect against tissue injury. Transforming growth factor-beta (TGF-beta) is a critical differentiation factor for the generation of T(reg) cells. Here we show, using mice with a reporter introduced into the endogenous Foxp3 locus, that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ T(reg) cells induced by TGF-beta. We also demonstrate that IL-23 is not the differentiation factor for the generation of T(H)17 cells. Instead, IL-6 and TGF-beta together induce the differentiation of pathogenic T(H)17 cells from naive T cells. Our data demonstrate a dichotomy in the generation of pathogenic (T(H)17) T cells that induce autoimmunity and regulatory (Foxp3+) T cells that inhibit autoimmune tissue injury.
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              The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

              Ivaylo Ivanov, Brent McKenzie, Liang Zhou … (2006)
              IL-17-producing T lymphocytes have been recently shown to comprise a distinct lineage of proinflammatory T helper cells, termed Th17 cells, that are major contributors to autoimmune disease. We show here that the orphan nuclear receptor RORgammat is the key transcription factor that orchestrates the differentiation of this effector cell lineage. RORgammat induces transcription of the genes encoding IL-17 and the related cytokine IL-17F in naïve CD4(+) T helper cells and is required for their expression in response to IL-6 and TGF-beta, the cytokines known to induce IL-17. Th17 cells are constitutively present throughout the intestinal lamina propria, express RORgammat, and are absent in mice deficient for RORgammat or IL-6. Mice with RORgammat-deficient T cells have attenuated autoimmune disease and lack tissue-infiltrating Th17 cells. Together, these studies suggest that RORgammat is a key regulator of immune homeostasis and highlight its potential as a therapeutic target in inflammatory diseases.
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                Author and article information

                Contributors
                Ning Gu:
                ORCID: https://orcid.org/0000-0003-0704-6768
                Journal
                Journal ID (nlm-ta): Dis Markers
                Journal ID (iso-abbrev): Dis Markers
                Journal ID (publisher-id): DM
                Title: Disease Markers
                Publisher: Hindawi
                ISSN (Print): 0278-0240
                ISSN (Electronic): 1875-8630
                Publication date Collection: 2020
                Publication date (Electronic): 31 October 2020
                Volume: 2020
                Electronic Location Identifier: 8821029
                Affiliations
                1Nanjing University of Chinese Medicine, Nanjing, China
                2Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing, China
                Author notes

                Academic Editor: Agata Sakowicz

                Author information
                https://orcid.org/0000-0002-2702-1632
                https://orcid.org/0000-0002-1749-6976
                https://orcid.org/0000-0003-0704-6768
                Article
                DOI: 10.1155/2020/8821029
                PMC ID: 7648711
                PubMed ID: 33193911
                SO-VID: 43222c2f-2caf-439a-af86-ce786e6d8e75
                Copyright © Copyright © 2020 Xin He et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 July 2020
                Date revision received : 30 September 2020
                Date accepted : 21 October 2020
                Funding
                Funded by: Jiangsu Universities Nursing Advantage Discipline Project
                Award ID: 2019YSHL095
                Funded by: Major Project of Nanjing Medical Science and Technology Development during 13 th Five-Year Plan
                Award ID: ZDX16013
                Funded by: Jiangsu Leading Talent Project of Traditional Chinese Medicine
                Award ID: 2018 No.4
                Funded by: National Natural Science Foundation of China
                Award ID: 81774229
                Categories
                Subject: Review Article

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