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  1. Artikel: The Influence of Sex Hormones and X Chromosome in Immune Responses.

    Anesi, Nina / Miquel, Charles-Henry / Laffont, Sophie / Guéry, Jean-Charles

    Current topics in microbiology and immunology

    2023  Band 441, Seite(n) 21–59

    Abstract: Males and females differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections and cancers. Cellular targets and molecular pathways underlying sexual dimorphism in immunity have started to emerge ... ...

    Abstract Males and females differ in their susceptibility to develop autoimmunity and allergy but also in their capacity to cope with infections and cancers. Cellular targets and molecular pathways underlying sexual dimorphism in immunity have started to emerge and appeared multifactorial. It became increasingly clear that sex-linked biological factors have important impact on the development, tissue maintenance and effector function acquisition of distinct immune cell populations, thereby regulating multiple layers of innate or adaptive immunity through distinct mechanisms. This review discusses the recent development in our understanding of the cell-intrinsic actions of biological factors linked to sex, sex hormones and sex chromosome complement, on immune cells, which may account for the sex differences in susceptibility to autoimmune diseases and allergies, and the sex-biased responses in natural immunity and cancer.
    Mesh-Begriff(e) Female ; Male ; Humans ; X Chromosome ; Gonadal Steroid Hormones/genetics ; Autoimmune Diseases/genetics ; Hypersensitivity ; Adaptive Immunity
    Chemische Substanzen Gonadal Steroid Hormones
    Sprache Englisch
    Erscheinungsdatum 2023-09-11
    Erscheinungsland Germany
    Dokumenttyp Review ; Journal Article
    ZDB-ID 210099-X
    ISSN 0070-217X
    ISSN 0070-217X
    DOI 10.1007/978-3-031-35139-6_2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Targeting androgen signaling in ILC2s protects from IL-33-driven lung inflammation, independently of KLRG1.

    Blanquart, Eve / Mandonnet, Audrey / Mars, Marion / Cenac, Claire / Anesi, Nina / Mercier, Pascale / Audouard, Christophe / Roga, Stephane / Serrano de Almeida, Gilberto / Bevan, Charlotte L / Girard, Jean-Philippe / Pelletier, Lucette / Laffont, Sophie / Guéry, Jean-Charles

    The Journal of allergy and clinical immunology

    2021  Band 149, Heft 1, Seite(n) 237–251.e12

    Abstract: Background: Allergic asthma is more severe and frequent in women than in men. In male mice, androgens negatively control group 2 innate lymphoid cell (ILC2) development and function by yet unknown mechanisms.: Objectives: We sought to investigate the ...

    Abstract Background: Allergic asthma is more severe and frequent in women than in men. In male mice, androgens negatively control group 2 innate lymphoid cell (ILC2) development and function by yet unknown mechanisms.
    Objectives: We sought to investigate the impact of androgen on ILC2 homeostasis and IL-33-mediated inflammation in female lungs. We evaluated the role of androgen receptor (AR) signaling and the contribution of the putative inhibitory receptor killer cell lectin-like receptor G1 (KLRG1).
    Methods: Subcutaneous pellets mimicking physiological levels of androgen were used to treat female mice together with mice expressing a reporter enzyme under the control of androgen response elements and mixed bone marrow chimeras to assess the cell-intrinsic role of AR activation within ILC2s. We generated KLRG1-deficient mice.
    Results: We established that lung ILC2s express a functionally active AR that can be in vivo targeted with exogenous androgens to negatively control ILC2 homeostasis, proliferation, and function. Androgen signaling upregulated KLRG1 on ILC2s, which inhibited their proliferation on E-cadherin interaction. Despite evidence that KLRG1 impaired the competitive fitness of lung ILC2s during inflammation, KLRG1 deficiency neither alters in vivo ILC2 numbers and functions, nor did it lead to hyperactive ILC2s in either sexes.
    Conclusions: AR agonists can be used in vivo to inhibit ILC2 homeostatic numbers and ILC2-dependent lung inflammation through cell-intrinsic AR activation. Although androgen signals in ILC2s to upregulate KLRG1, we demonstrate that KLRG1 is dispensable for androgen-mediated inhibition of pulmonary ILC2s.
    Mesh-Begriff(e) Androgens/pharmacology ; Animals ; Female ; Interleukin-33/immunology ; Lectins, C-Type/immunology ; Lung/immunology ; Lung/pathology ; Lymphocytes/immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Pneumonia/immunology ; Pneumonia/pathology ; Receptors, Immunologic/immunology ; Sex Characteristics ; Signal Transduction ; Testosterone/pharmacology ; Mice
    Chemische Substanzen Androgens ; Interleukin-33 ; Klrg1 protein, mouse ; Lectins, C-Type ; Receptors, Immunologic ; Testosterone (3XMK78S47O)
    Sprache Englisch
    Erscheinungsdatum 2021-05-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2021.04.029
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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