Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress
Inflammatory immune response plays a key role in reproductive failures such as multiple implantation failures (MIF), early pregnancy loss, and recurrent pregnancy losses (RPL). Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditi...
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| Veröffentlicht in: | American journal of reproductive immunology (1989) 2014-08, Vol.72 (2), p.129-140 |
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| container_title | American journal of reproductive immunology (1989) |
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| creator | Kwak-Kim, Joanne Bao, Shihua Lee, Sung Ki Kim, Joon Woo Gilman-Sachs, Alice |
| description | Inflammatory immune response plays a key role in reproductive failures such as multiple implantation failures (MIF), early pregnancy loss, and recurrent pregnancy losses (RPL). Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditions. Excessive or inappropriate recruitment of peripheral blood NK cells to the uterus may lead to cytotoxic environment in utero, in which proliferation and differentiation of trophoblast is hampered. In addition, inadequate angiogenesis by uterine NK cells often leads to abnormal vascular development and blood flow patterns, which, in turn, leads to increased oxidative stress or ischemic changes in the invading trophoblast. T‐cell abnormalities with increased Th1 and Th17 immunity, and decreased Th2 and T regulatory immune responses may play important roles in RPL and MIF. A possible role of stress in inflammatory immune response is also reviewed. |
| doi_str_mv | 10.1111/aji.12234 |
| format | Article |
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Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditions. Excessive or inappropriate recruitment of peripheral blood NK cells to the uterus may lead to cytotoxic environment in utero, in which proliferation and differentiation of trophoblast is hampered. In addition, inadequate angiogenesis by uterine NK cells often leads to abnormal vascular development and blood flow patterns, which, in turn, leads to increased oxidative stress or ischemic changes in the invading trophoblast. T‐cell abnormalities with increased Th1 and Th17 immunity, and decreased Th2 and T regulatory immune responses may play important roles in RPL and MIF. A possible role of stress in inflammatory immune response is also reviewed.</description><identifier>ISSN: 1046-7408</identifier><identifier>EISSN: 1600-0897</identifier><identifier>DOI: 10.1111/aji.12234</identifier><identifier>PMID: 24661472</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Abortion, Habitual - immunology ; Abortion, Habitual - pathology ; Angiogenesis ; Cytokines - biosynthesis ; Cytokines - immunology ; Embryo Loss - immunology ; Embryo Loss - pathology ; Female ; Humans ; Immune system ; Inflammation - immunology ; Inflammation - pathology ; Killer Cells, Natural - immunology ; Killer Cells, Natural - pathology ; Miscarriage ; multiple implantation failure ; natural killer cell ; Neovascularization, Pathologic ; Oxidative Stress ; Pregnancy ; recurrent pregnancy loss ; stress ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology ; Trophoblasts - immunology ; Trophoblasts - pathology ; uterine blood flow ; Uterus - blood supply ; Uterus - immunology ; Uterus - pathology</subject><ispartof>American journal of reproductive immunology (1989), 2014-08, Vol.72 (2), p.129-140</ispartof><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5604-79cdca3db27e4df7c3c2f5dfe02bf69566760b9972d0ee774160cddc38b762173</citedby><cites>FETCH-LOGICAL-c5604-79cdca3db27e4df7c3c2f5dfe02bf69566760b9972d0ee774160cddc38b762173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Faji.12234$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Faji.12234$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24661472$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwak-Kim, Joanne</creatorcontrib><creatorcontrib>Bao, Shihua</creatorcontrib><creatorcontrib>Lee, Sung Ki</creatorcontrib><creatorcontrib>Kim, Joon Woo</creatorcontrib><creatorcontrib>Gilman-Sachs, Alice</creatorcontrib><title>Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress</title><title>American journal of reproductive immunology (1989)</title><addtitle>Am J Reprod Immunol</addtitle><description>Inflammatory immune response plays a key role in reproductive failures such as multiple implantation failures (MIF), early pregnancy loss, and recurrent pregnancy losses (RPL). Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditions. Excessive or inappropriate recruitment of peripheral blood NK cells to the uterus may lead to cytotoxic environment in utero, in which proliferation and differentiation of trophoblast is hampered. In addition, inadequate angiogenesis by uterine NK cells often leads to abnormal vascular development and blood flow patterns, which, in turn, leads to increased oxidative stress or ischemic changes in the invading trophoblast. T‐cell abnormalities with increased Th1 and Th17 immunity, and decreased Th2 and T regulatory immune responses may play important roles in RPL and MIF. A possible role of stress in inflammatory immune response is also reviewed.</description><subject>Abortion, Habitual - immunology</subject><subject>Abortion, Habitual - pathology</subject><subject>Angiogenesis</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - immunology</subject><subject>Embryo Loss - immunology</subject><subject>Embryo Loss - pathology</subject><subject>Female</subject><subject>Humans</subject><subject>Immune system</subject><subject>Inflammation - immunology</subject><subject>Inflammation - pathology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - pathology</subject><subject>Miscarriage</subject><subject>multiple implantation failure</subject><subject>natural killer cell</subject><subject>Neovascularization, Pathologic</subject><subject>Oxidative Stress</subject><subject>Pregnancy</subject><subject>recurrent pregnancy loss</subject><subject>stress</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><subject>Trophoblasts - immunology</subject><subject>Trophoblasts - pathology</subject><subject>uterine blood flow</subject><subject>Uterus - blood supply</subject><subject>Uterus - immunology</subject><subject>Uterus - pathology</subject><issn>1046-7408</issn><issn>1600-0897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1LHTEUhkNpqVa76B8ogW4sOJqvSWbcibV6y71-0A_BTcgkJzLXmYlNZmjvv2_0qotCodkkhOd94JwXoXeU7NF89s2y3aOMcfECbVJJSEGqWr3MbyJkoQSpNtCblJaE5H-uXqMNJqSkQrFNdDnr-2kIXbhprenwIjhIOHh8EeFmMINd4XlI6QDPBt-ZvjdjG4Zd_BACfOw92DHEtIvN4PDXMUJK2-iVN12Ct4_3Fvr--fjb0WkxPz-ZHR3OC1tKIgpVW2cNdw1TIJxXllvmS-eBsMbLupRSSdLUtWKOACgl8mDWOcurRklGFd9CO2vvXQw_J0ij7ttkoevMAGFKmpYllbyq6-o_UKFKRikXGf3wF7oMUxzyIPdUSbJS8Ex9XFM25u1E8Poutr2JK02Jvq9E50r0QyWZff9onJoe3DP51EEG9tfAr7aD1b9N-vDL7ElZrBNtGuH3c8LEWy0VV6W-OjvRP64Xn04XFdeX_A_dpKJn</recordid><startdate>201408</startdate><enddate>201408</enddate><creator>Kwak-Kim, Joanne</creator><creator>Bao, Shihua</creator><creator>Lee, Sung Ki</creator><creator>Kim, Joon Woo</creator><creator>Gilman-Sachs, Alice</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201408</creationdate><title>Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress</title><author>Kwak-Kim, Joanne ; Bao, Shihua ; Lee, Sung Ki ; Kim, Joon Woo ; Gilman-Sachs, Alice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5604-79cdca3db27e4df7c3c2f5dfe02bf69566760b9972d0ee774160cddc38b762173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abortion, Habitual - immunology</topic><topic>Abortion, Habitual - pathology</topic><topic>Angiogenesis</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - immunology</topic><topic>Embryo Loss - immunology</topic><topic>Embryo Loss - pathology</topic><topic>Female</topic><topic>Humans</topic><topic>Immune system</topic><topic>Inflammation - immunology</topic><topic>Inflammation - pathology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - pathology</topic><topic>Miscarriage</topic><topic>multiple implantation failure</topic><topic>natural killer cell</topic><topic>Neovascularization, Pathologic</topic><topic>Oxidative Stress</topic><topic>Pregnancy</topic><topic>recurrent pregnancy loss</topic><topic>stress</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><topic>Trophoblasts - immunology</topic><topic>Trophoblasts - pathology</topic><topic>uterine blood flow</topic><topic>Uterus - blood supply</topic><topic>Uterus - immunology</topic><topic>Uterus - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwak-Kim, Joanne</creatorcontrib><creatorcontrib>Bao, Shihua</creatorcontrib><creatorcontrib>Lee, Sung Ki</creatorcontrib><creatorcontrib>Kim, Joon Woo</creatorcontrib><creatorcontrib>Gilman-Sachs, Alice</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of reproductive immunology (1989)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwak-Kim, Joanne</au><au>Bao, Shihua</au><au>Lee, Sung Ki</au><au>Kim, Joon Woo</au><au>Gilman-Sachs, Alice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress</atitle><jtitle>American journal of reproductive immunology (1989)</jtitle><addtitle>Am J Reprod Immunol</addtitle><date>2014-08</date><risdate>2014</risdate><volume>72</volume><issue>2</issue><spage>129</spage><epage>140</epage><pages>129-140</pages><issn>1046-7408</issn><eissn>1600-0897</eissn><abstract>Inflammatory immune response plays a key role in reproductive failures such as multiple implantation failures (MIF), early pregnancy loss, and recurrent pregnancy losses (RPL). Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditions. Excessive or inappropriate recruitment of peripheral blood NK cells to the uterus may lead to cytotoxic environment in utero, in which proliferation and differentiation of trophoblast is hampered. In addition, inadequate angiogenesis by uterine NK cells often leads to abnormal vascular development and blood flow patterns, which, in turn, leads to increased oxidative stress or ischemic changes in the invading trophoblast. T‐cell abnormalities with increased Th1 and Th17 immunity, and decreased Th2 and T regulatory immune responses may play important roles in RPL and MIF. A possible role of stress in inflammatory immune response is also reviewed.</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>24661472</pmid><doi>10.1111/aji.12234</doi><tpages>12</tpages></addata></record> |
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| subjects | Abortion, Habitual - immunology Abortion, Habitual - pathology Angiogenesis Cytokines - biosynthesis Cytokines - immunology Embryo Loss - immunology Embryo Loss - pathology Female Humans Immune system Inflammation - immunology Inflammation - pathology Killer Cells, Natural - immunology Killer Cells, Natural - pathology Miscarriage multiple implantation failure natural killer cell Neovascularization, Pathologic Oxidative Stress Pregnancy recurrent pregnancy loss stress T-Lymphocytes - immunology T-Lymphocytes - pathology Trophoblasts - immunology Trophoblasts - pathology uterine blood flow Uterus - blood supply Uterus - immunology Uterus - pathology |
| title | Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress |
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