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  1. Article ; Online: Androgen receptor signaling promotes Treg suppressive function during allergic airway inflammation

    Vivek D. Gandhi / Jacqueline-Yvonne Cephus / Allison E. Norlander / Nowrin U. Chowdhury / Jian Zhang / Zachary J. Ceneviva / Elie Tannous / Vasiliy V. Polosukhin / Nathan D. Putz / Nancy Wickersham / Amrit Singh / Lorraine B. Ware / Julie A. Bastarache / Ciara M. Shaver / Hong Wei Chu / R. Stokes Peebles Jr. / Dawn C. Newcomb

    The Journal of Clinical Investigation, Vol 132, Iss

    2022  Volume 4

    Abstract: Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ... ...

    Abstract Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ST2+ Tregs promote allergic airway inflammation. Clinical studies showed that the androgen dehydroepiandrosterone (DHEA) reduced asthma symptoms in patients, and mouse studies showed that androgen receptor (AR) signaling decreased allergic airway inflammation. Yet the impact of AR signaling on lung Tregs remains unclear. Using AR-deficient and Foxp3 fate-mapping mice, we determined that AR signaling increased Treg suppression during Alternaria extract (Alt Ext; allergen) challenge by stabilizing Foxp3+ Tregs and limiting the number of ST2+ ex-Tregs and IL-13+ Th2 cells and ex-Tregs. AR signaling also decreased Alt Ext–induced ST2+ Tregs in mice by limiting expression of Gata2, a transcription factor for ST2, and by decreasing Alt Ext–induced IL-33 production from murine airway epithelial cells. We confirmed our findings in human cells where 5α-dihydrotestosterone (DHT), an androgen, decreased IL-33–induced ST2 expression in lung Tregs and decreased Alt Ext–induced IL-33 secretion in human bronchial epithelial cells. Our findings showed that AR signaling stabilized Treg suppressive function, providing a mechanism for the sex difference in asthma.
    Keywords Inflammation ; Pulmonology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Testosterone Attenuates Group 2 Innate Lymphoid Cell-Mediated Airway Inflammation

    Jacqueline-Yvonne Cephus / Matthew T. Stier / Hubaida Fuseini / Jeffrey A. Yung / Shinji Toki / Melissa H. Bloodworth / Weisong Zhou / Kasia Goleniewska / Jian Zhang / Sarah L. Garon / Robert G. Hamilton / Vasiliy V. Poloshukin / Kelli L. Boyd / R. Stokes Peebles, Jr. / Dawn C. Newcomb

    Cell Reports, Vol 21, Iss 9, Pp 2487-

    2017  Volume 2499

    Abstract: Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we ... ...

    Abstract Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we investigate how testosterone attenuates ILC2 function. In patients with moderate to severe asthma, we determine that women have an increased number of circulating ILC2 compared to men. ILC2 from adult female mice have increased IL-2-mediated ILC2 proliferation versus ILC2 from adult male mice, as well as pre-pubescent females and males. Further, 5α-dihydrotestosterone, a hormone downstream of testosterone, decreases lung ILC2 numbers and IL-5 and IL-13 expression from ILC2. In vivo, testosterone attenuated Alternaria-extract-induced IL-5+ and IL-13+ ILC2 numbers and lung eosinophils by intrinsically decreasing lung ILC2 numbers, as well as by decreasing expression of IL-33 and thymic stromal lymphopoietin (TSLP), ILC2-stimulating cytokines. Collectively, these findings provide a foundational understanding of sexual dimorphism in ILC2 function.
    Keywords innate lymphoid cells ; testosterone ; sex hormones ; asthma ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2017-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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