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3208.Full.Pdf Retinoid-Related Orphan Receptor γ Controls Immunoglobulin Production and Th1/Th2 Cytokine Balance in the Adaptive Immune Response to Allergen This information is current as of September 25, 2021. Stephen L. Tilley, Maisa Jaradat, Cliona Stapleton, Darlene Dixon, Xiaoyang Hua, Christopher J. Erikson, Joshua G. McCaskill, Kelly D. Chason, Grace Liao, Leigh Jania, Beverly H. Koller and Anton M. Jetten J Immunol 2007; 178:3208-3218; ; Downloaded from doi: 10.4049/jimmunol.178.5.3208 http://www.jimmunol.org/content/178/5/3208 http://www.jimmunol.org/ References This article cites 52 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/178/5/3208.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 25, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Retinoid-Related Orphan Receptor ␥ Controls Immunoglobulin Production and Th1/Th2 Cytokine Balance in the Adaptive Immune Response to Allergen1 Stephen L. Tilley,2* Maisa Jaradat,‡ Cliona Stapleton,‡ Darlene Dixon,§ Xiaoyang Hua,* Christopher J. Erikson,* Joshua G. McCaskill,* Kelly D. Chason,* Grace Liao,‡ Leigh Jania,† Beverly H. Koller,† and Anton M. Jetten‡ The retinoid-related orphan receptors (ROR) comprise a distinct subfamily of nuclear receptors with the capacity to act as both repressors and activators of transcription. ROR␥, the most recently identified member of the ROR family, has been shown to be important for the development of normal lymphocyte compartments as well as organogenesis of some lymphoid organs. In this report, we examine the capacity of ROR␥-deficient mice to develop an adaptive immune response to Ag using OVA-induced Downloaded from inflammation in mice as a model for allergic airway disease. In sham-treated mice lacking ROR␥, low-grade pulmonary inflam- mation was observed and characterized by the perivascular accumulation of B and T lymphocytes, increased numbers of inflam- matory cells in the lung lavage fluid, and polyclonal Ig activation. Following sensitization and challenge, the capacity of these animals to develop the allergic phenotype was severely impaired as evidenced by attenuated eosinophilic pulmonary inflammation, ␥-reduced numbers of CD4؉ lymphocytes, and lower Th2 cytokines/chemokine protein and mRNA expression in the lungs. IFN and IL-10 production was markedly greater in splenocytes from ROR␥-deficient mice following in vitro restimulation with OVA http://www.jimmunol.org/ compared with wild-type splenocytes, and a shift toward a Th1 immune response was observed in sensitized/challenged ROR␥- deficient animals in vivo. These data reveal a critical role for ROR␥ in the regulation of Ig production and Th1/Th2 balance in adaptive immunity. The Journal of Immunology, 2007, 178: 3208–3218. uclear receptors constitute a superfamily of ligand-de- The ROR, ROR␣, ␤, and ␥, constitute a subfamily of nuclear pendent transcription factors that include receptors for orphan receptors whose roles in inflammation are less well under- N steroid hormones, retinoic acid, and thyroid hormone; stood. Similar to other nuclear receptors, ROR are believed to be and orphan receptors for which the ligands have yet to be identified activated by small lipophilic molecules that bind to the receptor, by guest on September 25, 2021 (1). Several studies have demonstrated a role for a number of nu- induce a conformational change resulting in the dissociation of clear receptors in the regulation of inflammation. These include the corepressor complexes, and facilitating translocation to the nucleus glucocorticoid receptor (GR),3 estrogen receptor, vitamin D recep- where gene expression is modulated. In addition to their capacity tor, retinoic acid receptors, peroxisome proliferator-activated re- to directly promote gene transcription, an anti-inflammatory role ceptors, and several orphan receptors, including members of the for ROR has been suggested based on findings that they can pos- retinoid-related orphan receptor (ROR) subfamily (2–11). The anti- itively regulate the expression of I␬B␣ (12). Thus, similar to GR, inflammatory action of glucocorticoids, ligands for the GR, is well ROR can act as both ligand-dependent transcription activators as established, and these agonists form the first line of treatment in well as ligand-dependent negative regulators of other transcription asthma. factors. Due in part to this complexity, the precise role of these receptors in inflammation has been difficult to predict. The newest member of the ROR subfamily, ROR␥, was first *Department of Medicine, Division of Pulmonary and Critical Care Medicine, and identified in skeletal muscle by its homology to retinoic acid re- †Department of Genetics University of North Carolina, Chapel Hill, NC 27599; and ‡ § ceptor but speculated to play a role in inflammation based upon its Laboratory of Respiratory Biology, Cell Biology Section, and Laboratory of Ex- ϩ ϩ perimental Pathology, Division of Intramural Research, National Institute of Envi- abundant expression in CD4 CD8 double-positive thymocytes ronmental Health Sciences, National Institutes of Health, Research Triangle Park, (13, 14). Forced expression of ROR␥ in T cell hybridomas resulted NC 27709 in inhibition of TCR-induced proliferation and cell death, suggest- Received for publication November 10, 2005. Accepted for publication December 12, 2006. ing an important role for this ROR subtype in T cell apoptosis (15, 16). Indeed, disruption of the ROR␥ gene in mice resulted in a The costs of publication of this article were defrayed in part by the payment of page ϩ ϩ charges. This article must therefore be hereby marked advertisement in accordance markedly increased rate of apoptosis in CD4 CD8 double-pos- with 18 U.S.C. Section 1734 solely to indicate this fact. itive thymocytes, confirming the physiological importance of 1 This work is supported by Intramural Research Program of the National Institute on ROR␥ in T cell biology in vivo (17, 18). Due to this accelerated Environmental Health Sciences, National Institutes of Health, and the extramural National Institutes of Health Grant HL071802. rate of apoptosis, the numbers of peripheral blood T lymphocytes 2 in ROR␥-deficient mice were decreased 6-fold, with a 10-fold re- Address correspondence and reprint requests to Stephen L. Tilley, 8033 Burnett- ϩ ϩ Womack, CB# 7219, University of North Carolina, Chapel Hill, NC 27599-7219. duction in CD4 cells and a 3-fold reduction in CD8 cells (17). E-mail address: [email protected] Despite a lower thymic output, T cells from ROR␥-deficient mice 3 Abbreviations used in this paper: GR, glucocorticoid receptor; EOS, eosinophil; appear to be exported normally to the periphery and have normal PAS, periodic acid-Schiff; PMN, polymorphonuclear neutrophil; Raw, airway resis- proliferative function (18). The numbers of CD4ϩ and CD8ϩ lym- tance; RL, dynamic resistance; ROR, retinoid-related orphan receptor; Th17, IL-17- producing Th. phocytes are normal to marginally increased in the spleens of www.jimmunol.org The Journal of Immunology 3209 FIGURE 1. Lung lavage fluid cel- lularity in wt and ROR␥Ϫ/Ϫ mice. Total cells and differentials were evaluated in sensitized mice 24 h following the last of five daily aerosol challenges with sa- line (A)orOVA(B). Saline-exposed ROR␥Ϫ/Ϫ (Ⅺ, n ϭ 15), saline- exposed wt (f, n ϭ 13), OVA- exposed ROR␥Ϫ/Ϫ (Ⅺ, n ϭ 14), and OVA-exposed wt (f, n ϭ 16). Data represent mean cell number Ϯ SEM. -p Ͻ 0.05. C, Representative cy ,ء tospin from saline-exposed wt mouse showing macrophages and a few lym- phocytes. D, Representative cytospin Ϫ/Ϫ from saline-exposed ROR␥ mouse Downloaded from showing granulocytes, lymphocytes, and macrophages. Slides were stained with Hema-3. http://www.jimmunol.org/ ROR␥-deficient mice, whereas the B cell compartment is substan- for 10 min at 4°C. The supernatants were aliquoted, 10% FBS was added tially expanded, ϳ3-fold the numbers found in wild-type (wt) con- to each aliquot, and samples subsequently frozen at Ϫ80°C for cytokine trols (19). In addition to these abnormalities in lymphocyte ho- analysis. Cell pellets were resuspended in 1 ml of HBSS and counted with ␥ a hemocytometer. Slides of lavage fluid cells were prepared using a Cy- meostasis, ROR -deficient mice fail to develop lymph nodes and tospin-3 centrifuge (Thermo Shandon) and stained with Mema-3 and Fast Peyer’s patches (17, 18). Based on these observations of abnor- Green (eosinophil stain) for determination of cellular differentials. malities in T cell homeostasis and lymphoid organogenesis, we Lung histopathology by guest on September 25, 2021 surmised that ROR␥-deficient mice might have an impaired ca- pacity to generate an adaptive immune response to Ag. To test this Immediately following whole-lung lavage, the lungs were inflated with 10% hypothesis, we compared the induction of inflammatory responses neutral-buffered formalin under 20 cm of pressure, and the trachea was tied off. ␥ The lungs were then removed en bloc, immersed in 10% formalin, and dehy- between wt and ROR -deficient mice using OVA-induced inflam- drated with ethanol before paraffin embedding. Five- to 6-␮m serial sections mation as a model system for allergic asthma. were cut through the right lung lobes and stained with H&E for general mor- phology and periodic acid-Schiff (PAS)/Alcian blue for mucus.
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