Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis
Identifieur interne : 000795 ( Pmc/Corpus ); précédent : 000794; suivant : 000796Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis
Auteurs : Dionne P. Robinson ; Sabra L. KleinSource :
- Hormones and behavior [ 0018-506X ] ; 2012.
Abstract
During pregnancy, it is evolutionary advantageous for inflammatory immune responses that might lead to fetal rejection to be reduced and anti-inflammatory responses that promote transfer of maternal antibodies to the fetus to be increased. Hormones modulate the immunological shift that occurs during pregnancy. Estrogens, including estradiol and estriol, progesterone, and glucocorticoids increase over the course of pregnancy and affect transcriptional signaling of inflammatory immune responses at the maternal-fetal interface and systemically. During pregnancy, the reduced activity of natural killer cells, inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of inflammatory cytokines, combined with the higher activity of regulatory T cells and production of anti-inflammatory cytokines, affects disease pathogenesis. The severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) is reduced and the severity of diseases that are mitigated by inflammatory responses (e.g., influenza and malaria) is increased during pregnancy. For some infectious diseases, elevated inflammatory responses that are necessary to control and clear a pathogen have a negative consequence on the outcome of pregnancy. The bidirectional interactions between hormones and the immune system contribute to both the outcome of pregnancy and female susceptibility to disease.
Url:
DOI: 10.1016/j.yhbeh.2012.02.023
PubMed: 22406114
PubMed Central: 3376705
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PMC:3376705Le document en format XML
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<author><name sortKey="Klein, Sabra L" sort="Klein, Sabra L" uniqKey="Klein S" first="Sabra L." last="Klein">Sabra L. Klein</name>
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<front><div type="abstract" xml:lang="en"><p id="P1">During pregnancy, it is evolutionary advantageous for inflammatory immune responses that might lead to fetal rejection to be reduced and anti-inflammatory responses that promote transfer of maternal antibodies to the fetus to be increased. Hormones modulate the immunological shift that occurs during pregnancy. Estrogens, including estradiol and estriol, progesterone, and glucocorticoids increase over the course of pregnancy and affect transcriptional signaling of inflammatory immune responses at the maternal-fetal interface and systemically. During pregnancy, the reduced activity of natural killer cells, inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of inflammatory cytokines, combined with the higher activity of regulatory T cells and production of anti-inflammatory cytokines, affects disease pathogenesis. The severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) is reduced and the severity of diseases that are mitigated by inflammatory responses (e.g., influenza and malaria) is increased during pregnancy. For some infectious diseases, elevated inflammatory responses that are necessary to control and clear a pathogen have a negative consequence on the outcome of pregnancy. The bidirectional interactions between hormones and the immune system contribute to both the outcome of pregnancy and female susceptibility to disease.</p>
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<title-group><article-title>Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Robinson</surname>
<given-names>Dionne P.</given-names>
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<contrib contrib-type="author"><name><surname>Klein</surname>
<given-names>Sabra L.</given-names>
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The W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205</aff>
<aff id="A2"><label>b</label>
Department of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205</aff>
<author-notes><corresp id="CR1">Correspondence: Sabra L. Klein The W. Harry Feinstone Department of Molecular Microbiology and Immunology The Johns Hopkins Bloomberg School of Public Health 615 N. Wolfe Street Baltimore, MD 21205 <email>saklein@jhsph.edu</email>
Telephone: (410) 955-8898 Fax: (410) 955-0105</corresp>
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<pub-date pub-type="nihms-submitted"><day>8</day>
<month>3</month>
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<pub-date pub-type="ppub"><month>8</month>
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<pub-date pub-type="pmc-release"><day>01</day>
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<volume>62</volume>
<issue>3</issue>
<fpage>263</fpage>
<lpage>271</lpage>
<permissions><copyright-statement>© 2012 Elsevier Inc. All rights reserved</copyright-statement>
<copyright-year>2012</copyright-year>
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<abstract><p id="P1">During pregnancy, it is evolutionary advantageous for inflammatory immune responses that might lead to fetal rejection to be reduced and anti-inflammatory responses that promote transfer of maternal antibodies to the fetus to be increased. Hormones modulate the immunological shift that occurs during pregnancy. Estrogens, including estradiol and estriol, progesterone, and glucocorticoids increase over the course of pregnancy and affect transcriptional signaling of inflammatory immune responses at the maternal-fetal interface and systemically. During pregnancy, the reduced activity of natural killer cells, inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of inflammatory cytokines, combined with the higher activity of regulatory T cells and production of anti-inflammatory cytokines, affects disease pathogenesis. The severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) is reduced and the severity of diseases that are mitigated by inflammatory responses (e.g., influenza and malaria) is increased during pregnancy. For some infectious diseases, elevated inflammatory responses that are necessary to control and clear a pathogen have a negative consequence on the outcome of pregnancy. The bidirectional interactions between hormones and the immune system contribute to both the outcome of pregnancy and female susceptibility to disease.</p>
</abstract>
<kwd-group><kwd>autoimmunity</kwd>
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<kwd>malaria</kwd>
<kwd>multiple sclerosis</kwd>
<kwd>progesterone</kwd>
<kwd>Th1/Th2</kwd>
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