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      The X-files in immunity: sex-based differences predispose immune responses

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      Publication date (Print):
      Journal: Nature Reviews. Immunology
      Publisher: Nature Publishing Group UK

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          Abstract

          Sex-based differences in immune responses can influence the susceptibility to autoimmune and infectious diseases and the efficacy of therapeutic drugs. In this Perspective, Eleanor Fish discusses factors, such as X-linked genes, hormones and societal context, that underlie disparate immune responses in men and women.

          Abstract

          Despite accumulating evidence in support of sex-based differences in innate and adaptive immune responses, in the susceptibility to infectious diseases and in the prevalence of autoimmune diseases, health research and clinical practice do not address these distinctions, and most research studies of immune responses do not stratify by sex. X-linked genes, hormones and societal context are among the many factors that contribute to disparate immune responses in males and females. It is crucial to address sex-based differences in disease pathogenesis and in the pharmacokinetics and pharmacodynamics of therapeutic medications to provide optimal disease management for both sexes.

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          Most cited references57

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          Sex differences in autoimmune disease.

          Caroline Whitacre (2001)
          Article 0 comments Cited 285 times – based on 0 reviews     Review now
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            Glycoprotein-D-adjuvant vaccine to prevent genital herpes.

            Pierre Vandepapeliere, , Fred Aoki … (2002)
            An effective prophylactic vaccine would help control the spread of genital herpes. We conducted two double-blind, randomized trials of a herpes simplex virus type 2 (HSV-2) glycoprotein-D-subunit vaccine with alum and 3-O-deacylated-monophosphoryl lipid A in subjects whose regular sexual partners had a history of genital herpes. In Study 1, subjects were seronegative for herpes simplex virus type 1 (HSV-1) and HSV-2; in Study 2, subjects were of any HSV serologic status. At months 0, 1, and 6, subjects received either vaccine or a control injection and were evaluated for 19 months. The primary end point was the occurrence of genital herpes disease in all subjects in Study 1 and in HSV-2-seronegative female subjects in Study 2. A total of 847 subjects who were seronegative for both HSV-1 and HSV-2 (268 of them women, in Study 1) and 1867 subjects who were seronegative for HSV-2 (710 of them women, in Study 2) underwent randomization and received injections. Vaccination was well tolerated and elicited humoral and cellular responses. Overall, the efficacy of the vaccine was 38 percent in Study 1 (95 percent confidence interval, -18 to 68 percent; 15 cases occurred in the vaccine group and 24 in the control group), and efficacy in female subjects was 42 percent in Study 2 (95 percent confidence interval, -31 to 74 percent; 9 cases occurred in the vaccine group and 16 in the control group). In both studies, further analysis showed that the vaccine was efficacious in women who were seronegative for both HSV-1 and HSV-2: efficacy in Study 1 was 73 percent (95 percent confidence interval, 19 to 91 percent; P=0.01), and efficacy in Study 2 was 74 percent (95 percent confidence interval, 9 to 93 percent; P=0.02). It was not efficacious in women who were seropositive for HSV-1 and seronegative for HSV-2 at base line or in men. These studies suggest that the glycoprotein D vaccine has efficacy against genital herpes in women who are seronegative for both HSV-1 and HSV-2 at base line but not in those who are seropositive for HSV-1 and seronegative for HSV-2. It had no efficacy in men, regardless of their HSV serologic status. Copyright 2002 Massachusetts Medical Society
            Article 0 comments Cited 130 times – based on 0 reviews     Review now
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              Testosterone reduces macrophage expression in the mouse of toll-like receptor 4, a trigger for inflammation and innate immunity.

              J Huet, Ian Marriott, A Rettew (2008)
              Though gender-based differences in the development of protective or pathological adaptive host responses have been widely noted, it is becoming apparent that sex may also influence the early perception of microbial challenges and the generation of inflammatory immune responses. These differences may be due to the actions of reproductive hormones, and such a hypothesis is supported by the presence of receptors for these hormones in a variety of immune cell types. Androgens such as testosterone have been shown to decrease immune functions, including cytokine production. However, the mechanisms by which testosterone limits such responses remain undefined. In this study, we have investigated the acute effects of testosterone on the level of expression of a key trigger for inflammation and innate immunity, Toll-like receptor 4 (TLR4), on isolated mouse macrophages. We show that in vitro testosterone treatment of macrophages, generated in the absence of androgen, elicits a modest but significant decrease in TLR4 expression and sensitivity to a TLR4-specific ligand. In addition, we have studied the effect of in vivo removal of endogenous testosterone on TLR4 expression and endotoxin susceptibility. We report that orchidectomized mice were significantly more susceptible to endotoxic shock and show that macrophages isolated from these animals have significantly higher TLR4 cell surface expression than those derived from sham gonadectomized mice. Importantly, these effects were not apparent in orchidectomized animals that received exogenous testosterone treatment. As such, these data may represent an important mechanism underlying the immunosuppressive effects of testosterone.
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                Author and article information

                Contributors
                Eleanor N. Fish:
                Bio :

                Eleanor Fish completed her m.Phil. in virology at the University of London, England, and her Ph.D. in cell biology at the Institute of medical Science at the University of Toronto, Canada. She is currently a professor in the Department of Immunology at the University of Toronto and Senior Scientist at the Toronto General Research Institute of the University Health Network, Toronto, Canada. The research activities of her laboratory include the study of cytokine and chemokine biology that is relevant to host–pathogen interactions and to autoimmune diseases.

                Journal
                Journal ID (nlm-ta): Nat Rev Immunol
                Journal ID (iso-abbrev): Nat. Rev. Immunol
                Title: Nature Reviews. Immunology
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 1474-1733
                ISSN (Electronic): 1474-1741
                Publication date (Print): 2008
                Volume: 8
                Issue: 9
                Pages: 737-744
                Affiliations
                GRID grid.17063.33, ISNI 0000 0001 2157 2938, Department of Immunology, , Eleanor N. Fish is at the Toronto General Research Institute, University Health Network, University of Toronto, Women's College Research Institute, 67, College Street, Toronto Ontario M5G 2M1, Canada. en.fish@utoronto.ca, ; ,
                Article
                Publisher ID: BFnri2394
                DOI: 10.1038/nri2394
                PMC ID: 7097214
                PubMed ID: 18728636
                SO-VID: 6c433b4e-4eef-4553-afff-7d0f8e1394d7
                Copyright © © Nature Publishing Group 2008
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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