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      Retinoic Acid-Related Orphan Receptors (RORs): Regulatory Functions in Immunity, Development, Circadian Rhythm, and Metabolism

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          Abstract

          In this overview, we provide an update on recent progress made in understanding the mechanisms of action, physiological functions, and roles in disease of retinoic acid related orphan receptors (RORs). We are particularly focusing on their roles in the regulation of adaptive and innate immunity, brain function, retinal development, cancer, glucose and lipid metabolism, circadian rhythm, metabolic and inflammatory diseases and neuropsychiatric disorders. We also summarize the current status of ROR agonists and inverse agonists, including their regulation of ROR activity and their therapeutic potential for management of various diseases in which RORs have been implicated.

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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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            TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

            Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
            We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
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              The orphan nuclear receptor REV-ERBalpha controls circadian transcription within the positive limb of the mammalian circadian oscillator.

              Nicolas Preitner, Francesca Damiola, Luis-Lopez-Molina … (2002)
              Mammalian circadian rhythms are generated by a feedback loop in which BMAL1 and CLOCK, players of the positive limb, activate transcription of the cryptochrome and period genes, components of the negative limb. Bmal1 and Per transcription cycles display nearly opposite phases and are thus governed by different mechanisms. Here, we identify the orphan nuclear receptor REV-ERBalpha as the major regulator of cyclic Bmal1 transcription. Circadian Rev-erbalpha expression is controlled by components of the general feedback loop. Thus, REV-ERBalpha constitutes a molecular link through which components of the negative limb drive antiphasic expression of components of the positive limb. While REV-ERBalpha influences the period length and affects the phase-shifting properties of the clock, it is not required for circadian rhythm generation.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101633889
                Journal ID (pubmed-jr-id): 42679
                Journal ID (nlm-ta): Nucl Receptor Res
                Journal ID (iso-abbrev): Nucl Receptor Res
                Title: Nuclear receptor research
                ISSN (Print): 2314-5706
                ISSN (Electronic): 2314-5714
                Publication date Nihms-submitted: 22 December 2015
                Publication date (Electronic): 16 December 2015
                Publication date (Print): 2015
                Publication date PMC-release: 11 February 2016
                Volume: 2
                Electronic Location Identifier: 101185
                Affiliations
                [1 ]Immunogenetics Section, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
                [2 ]Cell Biology Section, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
                Author notes
                Corresponding Author: Anton Jetten; jetten@ 123456niehs.nih.gov
                Article
                Manuscript ID: NIHMS746408
                DOI: 10.11131/2015/101185
                PMC ID: 4750502
                PubMed ID: 26878025
                SO-VID: 01932981-4649-4855-b89b-1b017a91a2ec
                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
                Categories
                Subject: Article

                Keywords: retinoic acid-related orphan receptor,rorγ,rorα,rorβ,immunity,th17 cells,innate lymphoid cells,autoimmune disease,retina,brain,cancer,metabolism,glucose homeostasis,lipid metabolism,insulin sensitivity,diabetes,circadian clock,agonists,cholesterol biosynthesis,autism,antagonist,transcription
                Data availability:
                Keywords: retinoic acid-related orphan receptor, rorγ, rorα, rorβ, immunity, th17 cells, innate lymphoid cells, autoimmune disease, retina, brain, cancer, metabolism, glucose homeostasis, lipid metabolism, insulin sensitivity, diabetes, circadian clock, agonists, cholesterol biosynthesis, autism, antagonist, transcription

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