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Crosstalk between estrogen, dendritic cells, and SARS‐CoV‐2 infection
The novel coronavirus disease 2019 (Covid‐19) first appeared in Wuhan and has so far killed more than four million people worldwide. Men are more affected than women by Covid‐19, but the cellular and molecular mechanisms behind these differences are largely unknown. One plausible explanation is that...
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Published in: | Reviews in Medical Virology 2022-05, Vol.32 (3), p.e2290-n/a |
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description | The novel coronavirus disease 2019 (Covid‐19) first appeared in Wuhan and has so far killed more than four million people worldwide. Men are more affected than women by Covid‐19, but the cellular and molecular mechanisms behind these differences are largely unknown. One plausible explanation is that differences in sex hormones could partially account for this distinct prevalence in both sexes. Accordingly, several papers have reported a protective role of 17β‐estradiol during Covid‐19, which might help explain why women appear less likely to die from Covid‐19 than men. 17β‐estradiol is the predominant and most biologically active endogenous estrogen, which signals through estrogen receptor α, estrogen receptor β, and G protein‐coupled estrogen receptor 1. These receptors are expressed in mature cells from the innate and the adaptive immune system, particularly on dendritic cells (DCs), suggesting that estrogens could modulate their effector functions. DCs are the most specialized and proficient antigen‐presenting cells, acting at the interface of innate and adaptive immunity with a powerful capacity to prime antigen‐specific naive CD8+ T cells. DCs are richly abundant in the lung where they respond to viral infection. A relative increase of mature DCs in broncho‐alveolar lavage fluids from Covid‐19 patients has already been reported. Here we will describe how SARS‐CoV‐2 acts on DCs, the role of estrogen on DC immunobiology, summarise the impact of sex hormones on the immune response against Covid‐19, and explore clinical trials regarding Covid‐19 |
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Men are more affected than women by Covid‐19, but the cellular and molecular mechanisms behind these differences are largely unknown. One plausible explanation is that differences in sex hormones could partially account for this distinct prevalence in both sexes. Accordingly, several papers have reported a protective role of 17β‐estradiol during Covid‐19, which might help explain why women appear less likely to die from Covid‐19 than men. 17β‐estradiol is the predominant and most biologically active endogenous estrogen, which signals through estrogen receptor α, estrogen receptor β, and G protein‐coupled estrogen receptor 1. These receptors are expressed in mature cells from the innate and the adaptive immune system, particularly on dendritic cells (DCs), suggesting that estrogens could modulate their effector functions. DCs are the most specialized and proficient antigen‐presenting cells, acting at the interface of innate and adaptive immunity with a powerful capacity to prime antigen‐specific naive CD8+ T cells. DCs are richly abundant in the lung where they respond to viral infection. A relative increase of mature DCs in broncho‐alveolar lavage fluids from Covid‐19 patients has already been reported. Here we will describe how SARS‐CoV‐2 acts on DCs, the role of estrogen on DC immunobiology, summarise the impact of sex hormones on the immune response against Covid‐19, and explore clinical trials regarding Covid‐19</description><identifier>ISSN: 1052-9276</identifier><identifier>ISSN: 1099-1654</identifier><identifier>EISSN: 1099-1654</identifier><identifier>DOI: 10.1002/rmv.2290</identifier><identifier>PMID: 34534372</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>17β-Estradiol ; Adaptive immunity ; Alveoli ; Antigen-presenting cells ; Antigens ; Biological activity ; CD8 antigen ; Clinical trials ; Coronaviruses ; COVID-19 ; Dendritic Cells ; Estradiol ; estrogen ; Estrogen receptors ; Estrogens ; Female ; Humans ; Lymphocytes T ; Male ; Molecular modelling ; Review ; Reviews ; SARS-CoV-2 ; Severe acute respiratory syndrome coronavirus 2 ; Sex hormones</subject><ispartof>Reviews in Medical Virology, 2022-05, Vol.32 (3), p.e2290-n/a</ispartof><rights>2021 John Wiley & Sons Ltd.</rights><rights>2021. 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Men are more affected than women by Covid‐19, but the cellular and molecular mechanisms behind these differences are largely unknown. One plausible explanation is that differences in sex hormones could partially account for this distinct prevalence in both sexes. Accordingly, several papers have reported a protective role of 17β‐estradiol during Covid‐19, which might help explain why women appear less likely to die from Covid‐19 than men. 17β‐estradiol is the predominant and most biologically active endogenous estrogen, which signals through estrogen receptor α, estrogen receptor β, and G protein‐coupled estrogen receptor 1. These receptors are expressed in mature cells from the innate and the adaptive immune system, particularly on dendritic cells (DCs), suggesting that estrogens could modulate their effector functions. DCs are the most specialized and proficient antigen‐presenting cells, acting at the interface of innate and adaptive immunity with a powerful capacity to prime antigen‐specific naive CD8+ T cells. DCs are richly abundant in the lung where they respond to viral infection. A relative increase of mature DCs in broncho‐alveolar lavage fluids from Covid‐19 patients has already been reported. Here we will describe how SARS‐CoV‐2 acts on DCs, the role of estrogen on DC immunobiology, summarise the impact of sex hormones on the immune response against Covid‐19, and explore clinical trials regarding Covid‐19</description><subject>17β-Estradiol</subject><subject>Adaptive immunity</subject><subject>Alveoli</subject><subject>Antigen-presenting cells</subject><subject>Antigens</subject><subject>Biological activity</subject><subject>CD8 antigen</subject><subject>Clinical trials</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>Dendritic Cells</subject><subject>Estradiol</subject><subject>estrogen</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Female</subject><subject>Humans</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Molecular modelling</subject><subject>Review</subject><subject>Reviews</subject><subject>SARS-CoV-2</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Sex hormones</subject><issn>1052-9276</issn><issn>1099-1654</issn><issn>1099-1654</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>COVID</sourceid><recordid>eNp9kd9qFTEQxoMotlbBJ5AFb7zo1sls_u2NUA5qCxWh1d6GZDdbU_ckbbKnpXd9hD6jT9KsrQcVWgKZwPz4Jt98hLymsEMB8H1aXuwgtvCEbFJo25oKzp7Ob451i1JskBc5nwLQcthzstEw3rBG4ibZX6SY82TGn5V106VzoXJ5SvHEhe2qd6FPfvJd1blxzNuVCX11tHt49Ov6ZhGPy42VD4PrJh_DS_JsMGN2r-7rFvn-6eO3xV598PXz_mL3oO6YEFAjUAWqEyiHoTVCoVDWKtMYJ6yFwTYInQXXguEGJSqQzCnOe2gtY4Nqmi3y4U73bGWXru9cmJIZ9VnyS5OudDRe_9sJ_oc-iRdaCSYY0iLw7l4gxfNVcauXPs8GTXBxlTVyyRhw2kJB3_6HnsZVCsWeRiE4cEVRPUpx2UiQopT12G7eeHLD-ssU9JyiLinqOcWCvvnb4hr8E1sB6jvg0o_u6kEhffjl-LfgLeYKpeU</recordid><startdate>202205</startdate><enddate>202205</enddate><creator>Mateus, Daniela</creator><creator>Sebastião, Ana Isabel</creator><creator>Carrascal, Mylène A.</creator><creator>Carmo, Anália do</creator><creator>Matos, Ana Miguel</creator><creator>Cruz, Maria Teresa</creator><general>John Wiley & Sons, Inc</general><general>Wiley Periodicals Inc</general><general>John Wiley and Sons Inc</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>COVID</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7511-4358</orcidid></search><sort><creationdate>202205</creationdate><title>Crosstalk between estrogen, dendritic cells, and SARS‐CoV‐2 infection</title><author>Mateus, Daniela ; Sebastião, Ana Isabel ; Carrascal, Mylène A. ; Carmo, Anália do ; Matos, Ana Miguel ; Cruz, Maria Teresa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4660-201808c627ff9a68268bb8a3ae6bb0fb320cb0e90a5a2728074e855d09b44f833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>17β-Estradiol</topic><topic>Adaptive immunity</topic><topic>Alveoli</topic><topic>Antigen-presenting cells</topic><topic>Antigens</topic><topic>Biological activity</topic><topic>CD8 antigen</topic><topic>Clinical trials</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>Dendritic Cells</topic><topic>Estradiol</topic><topic>estrogen</topic><topic>Estrogen receptors</topic><topic>Estrogens</topic><topic>Female</topic><topic>Humans</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Molecular modelling</topic><topic>Review</topic><topic>Reviews</topic><topic>SARS-CoV-2</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Sex hormones</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mateus, Daniela</creatorcontrib><creatorcontrib>Sebastião, Ana Isabel</creatorcontrib><creatorcontrib>Carrascal, Mylène A.</creatorcontrib><creatorcontrib>Carmo, Anália do</creatorcontrib><creatorcontrib>Matos, Ana Miguel</creatorcontrib><creatorcontrib>Cruz, Maria Teresa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Coronavirus Research Database</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Reviews in Medical Virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Mateus, Daniela</au><au>Sebastião, Ana Isabel</au><au>Carrascal, Mylène A.</au><au>Carmo, Anália do</au><au>Matos, Ana Miguel</au><au>Cruz, Maria Teresa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Crosstalk between estrogen, dendritic cells, and SARS‐CoV‐2 infection</atitle><jtitle>Reviews in Medical Virology</jtitle><addtitle>Rev Med Virol</addtitle><date>2022-05</date><risdate>2022</risdate><volume>32</volume><issue>3</issue><spage>e2290</spage><epage>n/a</epage><pages>e2290-n/a</pages><issn>1052-9276</issn><issn>1099-1654</issn><eissn>1099-1654</eissn><abstract>The novel coronavirus disease 2019 (Covid‐19) first appeared in Wuhan and has so far killed more than four million people worldwide. Men are more affected than women by Covid‐19, but the cellular and molecular mechanisms behind these differences are largely unknown. One plausible explanation is that differences in sex hormones could partially account for this distinct prevalence in both sexes. Accordingly, several papers have reported a protective role of 17β‐estradiol during Covid‐19, which might help explain why women appear less likely to die from Covid‐19 than men. 17β‐estradiol is the predominant and most biologically active endogenous estrogen, which signals through estrogen receptor α, estrogen receptor β, and G protein‐coupled estrogen receptor 1. These receptors are expressed in mature cells from the innate and the adaptive immune system, particularly on dendritic cells (DCs), suggesting that estrogens could modulate their effector functions. DCs are the most specialized and proficient antigen‐presenting cells, acting at the interface of innate and adaptive immunity with a powerful capacity to prime antigen‐specific naive CD8+ T cells. DCs are richly abundant in the lung where they respond to viral infection. A relative increase of mature DCs in broncho‐alveolar lavage fluids from Covid‐19 patients has already been reported. Here we will describe how SARS‐CoV‐2 acts on DCs, the role of estrogen on DC immunobiology, summarise the impact of sex hormones on the immune response against Covid‐19, and explore clinical trials regarding Covid‐19</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>34534372</pmid><doi>10.1002/rmv.2290</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-7511-4358</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | 17β-Estradiol Adaptive immunity Alveoli Antigen-presenting cells Antigens Biological activity CD8 antigen Clinical trials Coronaviruses COVID-19 Dendritic Cells Estradiol estrogen Estrogen receptors Estrogens Female Humans Lymphocytes T Male Molecular modelling Review Reviews SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Sex hormones |
title | Crosstalk between estrogen, dendritic cells, and SARS‐CoV‐2 infection |
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