Estrogen, estrogen-like molecules and autoimmune diseases
In western countries, the slope of autoimmune disease (AD) incidence is increasing and affects 5–8% of the population. Mainly prevalent in women, these pathologies are due to thymic tolerance processes breakdown. The female sex hormone, estrogen, is involved in this AD female susceptibility. However...
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| Veröffentlicht in: | Autoimmunity reviews 2020-03, Vol.19 (3), p.102468, Article 102468 |
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| container_title | Autoimmunity reviews |
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| creator | Merrheim, Judith Villegas, José Van Wassenhove, Jérôme Khansa, Rémi Berrih-Aknin, Sonia le Panse, Rozen Dragin, Nadine |
| description | In western countries, the slope of autoimmune disease (AD) incidence is increasing and affects 5–8% of the population. Mainly prevalent in women, these pathologies are due to thymic tolerance processes breakdown. The female sex hormone, estrogen, is involved in this AD female susceptibility. However, predisposition factors have to act in concert with unknown triggering environmental factors (virus, microbiota, pollution) to initiate AD. Individuals are exposed to various environmental compounds that display endocrine disruption abilities. The cellular effects of some of these molecules may be mediated through the aryl hydrocarbon receptor (AhR). Here, we review the effects of these molecules on the homeostasis of the thymic cells, the immune tolerance intrinsic factors (transcription factors, epigenetic marks) and on the immune tolerance extrinsic factors (microbiota, virus sensibility). This review highlights the contribution of estrogen and endocrine disruptors on the dysregulation of mechanisms sustaining AD development. |
| doi_str_mv | 10.1016/j.autrev.2020.102468 |
| format | Article |
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Mainly prevalent in women, these pathologies are due to thymic tolerance processes breakdown. The female sex hormone, estrogen, is involved in this AD female susceptibility. However, predisposition factors have to act in concert with unknown triggering environmental factors (virus, microbiota, pollution) to initiate AD. Individuals are exposed to various environmental compounds that display endocrine disruption abilities. The cellular effects of some of these molecules may be mediated through the aryl hydrocarbon receptor (AhR). Here, we review the effects of these molecules on the homeostasis of the thymic cells, the immune tolerance intrinsic factors (transcription factors, epigenetic marks) and on the immune tolerance extrinsic factors (microbiota, virus sensibility). 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Mainly prevalent in women, these pathologies are due to thymic tolerance processes breakdown. The female sex hormone, estrogen, is involved in this AD female susceptibility. However, predisposition factors have to act in concert with unknown triggering environmental factors (virus, microbiota, pollution) to initiate AD. Individuals are exposed to various environmental compounds that display endocrine disruption abilities. The cellular effects of some of these molecules may be mediated through the aryl hydrocarbon receptor (AhR). Here, we review the effects of these molecules on the homeostasis of the thymic cells, the immune tolerance intrinsic factors (transcription factors, epigenetic marks) and on the immune tolerance extrinsic factors (microbiota, virus sensibility). This review highlights the contribution of estrogen and endocrine disruptors on the dysregulation of mechanisms sustaining AD development.</description><subject>Animal models</subject><subject>Autoimmune Diseases - immunology</subject><subject>Disease susceptibility</subject><subject>Endocrine Disruptors - adverse effects</subject><subject>Estrogens - immunology</subject><subject>Female</subject><subject>Gender</subject><subject>Humans</subject><subject>Immune Tolerance</subject><subject>Life Sciences</subject><subject>Receptors, Aryl Hydrocarbon</subject><subject>Thymus</subject><subject>Thymus Gland - drug effects</subject><issn>1568-9972</issn><issn>1568-9972</issn><issn>1873-0183</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotlb_gcheBbcm2exuchFKqR9Q8KLnME1mNXU_SrJb8N-7y9biydMMw_vMMA8h14zOGWXZ_XYOXetxP-eUDyMuMnlCpizNZKxUzk__9BNyEcKW9pji6pxMEqZ4TmU2JWoVWt98YH0X4aGLS_eFUdWUaLoSQwS1jfpTjauqrsbIuoAQMFySswLKgFeHOiPvj6u35XO8fn16WS7WsRGCtzEkMkNKgRkOLC2QybTgoJIssZYXggsFgiLdWFA5E8wayJmVQM2mMIZnmMzI7bj3E0q9864C_60bcPp5sdbDjCaSC5qme9ZnxZg1vgnBY3EEGNWDNb3VozU9WNOjtR67GbFdt6nQHqFfTX3gYQxg_-jeodfBOKwNWufRtNo27v8LP_n8f5s</recordid><startdate>202003</startdate><enddate>202003</enddate><creator>Merrheim, Judith</creator><creator>Villegas, José</creator><creator>Van Wassenhove, Jérôme</creator><creator>Khansa, Rémi</creator><creator>Berrih-Aknin, Sonia</creator><creator>le Panse, Rozen</creator><creator>Dragin, Nadine</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-7522-5974</orcidid></search><sort><creationdate>202003</creationdate><title>Estrogen, estrogen-like molecules and autoimmune diseases</title><author>Merrheim, Judith ; Villegas, José ; Van Wassenhove, Jérôme ; Khansa, Rémi ; Berrih-Aknin, Sonia ; le Panse, Rozen ; Dragin, Nadine</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-a386e00a1c2a15fe185f2a9363dd2f4249a40e0bda97141dca71d8a0cbfcc26e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animal models</topic><topic>Autoimmune Diseases - immunology</topic><topic>Disease susceptibility</topic><topic>Endocrine Disruptors - adverse effects</topic><topic>Estrogens - immunology</topic><topic>Female</topic><topic>Gender</topic><topic>Humans</topic><topic>Immune Tolerance</topic><topic>Life Sciences</topic><topic>Receptors, Aryl Hydrocarbon</topic><topic>Thymus</topic><topic>Thymus Gland - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Merrheim, Judith</creatorcontrib><creatorcontrib>Villegas, José</creatorcontrib><creatorcontrib>Van Wassenhove, Jérôme</creatorcontrib><creatorcontrib>Khansa, Rémi</creatorcontrib><creatorcontrib>Berrih-Aknin, Sonia</creatorcontrib><creatorcontrib>le Panse, Rozen</creatorcontrib><creatorcontrib>Dragin, Nadine</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Autoimmunity reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Merrheim, Judith</au><au>Villegas, José</au><au>Van Wassenhove, Jérôme</au><au>Khansa, Rémi</au><au>Berrih-Aknin, Sonia</au><au>le Panse, Rozen</au><au>Dragin, Nadine</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen, estrogen-like molecules and autoimmune diseases</atitle><jtitle>Autoimmunity reviews</jtitle><addtitle>Autoimmun Rev</addtitle><date>2020-03</date><risdate>2020</risdate><volume>19</volume><issue>3</issue><spage>102468</spage><pages>102468-</pages><artnum>102468</artnum><issn>1568-9972</issn><eissn>1568-9972</eissn><eissn>1873-0183</eissn><abstract>In western countries, the slope of autoimmune disease (AD) incidence is increasing and affects 5–8% of the population. Mainly prevalent in women, these pathologies are due to thymic tolerance processes breakdown. The female sex hormone, estrogen, is involved in this AD female susceptibility. However, predisposition factors have to act in concert with unknown triggering environmental factors (virus, microbiota, pollution) to initiate AD. Individuals are exposed to various environmental compounds that display endocrine disruption abilities. The cellular effects of some of these molecules may be mediated through the aryl hydrocarbon receptor (AhR). Here, we review the effects of these molecules on the homeostasis of the thymic cells, the immune tolerance intrinsic factors (transcription factors, epigenetic marks) and on the immune tolerance extrinsic factors (microbiota, virus sensibility). 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| subjects | Animal models Autoimmune Diseases - immunology Disease susceptibility Endocrine Disruptors - adverse effects Estrogens - immunology Female Gender Humans Immune Tolerance Life Sciences Receptors, Aryl Hydrocarbon Thymus Thymus Gland - drug effects |
| title | Estrogen, estrogen-like molecules and autoimmune diseases |
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