Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome
Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease...
Gespeichert in:
| Veröffentlicht in: | Seminars in immunopathology 2022-05, Vol.44 (3), p.347-362 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 362 |
|---|---|
| container_issue | 3 |
| container_start_page | 347 |
| container_title | Seminars in immunopathology |
| container_volume | 44 |
| creator | Knight, Jason S. Kanthi, Yogendra |
| description | Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease but also key drivers of APS pathophysiology. Thrombotic events in APS can be attributed to various conspirators including activated endothelial cells, platelets, and myeloid-lineage cells, as well as derangements in coagulation and fibrinolytic systems. Furthermore, recent work has especially highlighted the role of neutrophil extracellular traps (NETs) and the complement system in APS thrombosis. Beyond acute thrombosis, patients with APS can also develop an occlusive vasculopathy, a long-term consequence of APS characterized by cell proliferation and infiltration that progressively expands the intima and leads to organ damage. This review will highlight known pathogenic factors in APS and will also briefly discuss similarities between APS and the thrombophilic coagulopathy of COVID-19. |
| doi_str_mv | 10.1007/s00281-022-00916-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8816310</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2626015342</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-50f4507eaefe800b3a56459ecd0bbb3212430a60bd2ea0877bf520a8829b15e43</originalsourceid><addsrcrecordid>eNp9kU9P3DAQxa2qqPxpv0APVaReegmM7ThxLpUqRAFpERc4W3biEKPETj0JaL89hl22pQcO1lie33ue0SPkK4VjClCdIACTNAfGcoCalvnjB3JAZclzxgE-vt5ZXe2TQ8R7AFFxUX0i-1xQxigtD8jqyja99g5HzEKXuXFcfJj7GEYT0GGmfZs9aGyWIUx67teZ8-ltdlMfMJ3BTa7NcO3bpLCfyV6nB7RftvWI3P4-uzm9yFfX55env1Z5U1TFnAvoCgGV1bazEsBwLcpC1LZpwRjDGWUFB12CaZnVIKvKdIKBlpLVhgpb8CPyc-M7LWa0bWP9HPWgpuhGHdcqaKfedrzr1V14UFLSklNIBj-2BjH8WSzOanTY2GHQ3oYFFStZCVTwgiX0-3_ofViiT-slSshaCip5otiGamJAjLbbDUNBPYelNmGpFJZ6CUs9JtG3f9fYSV7TSQDfAJha_s7Gv3-_Y_sEGkWh6w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2658985183</pqid></control><display><type>article</type><title>Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Knight, Jason S. ; Kanthi, Yogendra</creator><creatorcontrib>Knight, Jason S. ; Kanthi, Yogendra</creatorcontrib><description>Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease but also key drivers of APS pathophysiology. Thrombotic events in APS can be attributed to various conspirators including activated endothelial cells, platelets, and myeloid-lineage cells, as well as derangements in coagulation and fibrinolytic systems. Furthermore, recent work has especially highlighted the role of neutrophil extracellular traps (NETs) and the complement system in APS thrombosis. Beyond acute thrombosis, patients with APS can also develop an occlusive vasculopathy, a long-term consequence of APS characterized by cell proliferation and infiltration that progressively expands the intima and leads to organ damage. This review will highlight known pathogenic factors in APS and will also briefly discuss similarities between APS and the thrombophilic coagulopathy of COVID-19.</description><identifier>ISSN: 1863-2297</identifier><identifier>EISSN: 1863-2300</identifier><identifier>DOI: 10.1007/s00281-022-00916-w</identifier><identifier>PMID: 35122116</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Antibodies, Antiphospholipid ; Antiphospholipid antibodies ; Antiphospholipid syndrome ; Antiphospholipid Syndrome - complications ; Antiphospholipid Syndrome - diagnosis ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; Cell proliferation ; Complement activation ; COVID-19 ; COVID-19 - complications ; Endothelial Cells ; Fibrin ; Humans ; Immunology ; Internal Medicine ; Leukocytes (neutrophilic) ; Pathology ; Phospholipids ; Review ; Thromboinflammation ; Thrombophilia ; Thrombosis ; Thrombosis - complications ; Vascular Diseases</subject><ispartof>Seminars in immunopathology, 2022-05, Vol.44 (3), p.347-362</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-50f4507eaefe800b3a56459ecd0bbb3212430a60bd2ea0877bf520a8829b15e43</citedby><cites>FETCH-LOGICAL-c474t-50f4507eaefe800b3a56459ecd0bbb3212430a60bd2ea0877bf520a8829b15e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00281-022-00916-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00281-022-00916-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35122116$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Knight, Jason S.</creatorcontrib><creatorcontrib>Kanthi, Yogendra</creatorcontrib><title>Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome</title><title>Seminars in immunopathology</title><addtitle>Semin Immunopathol</addtitle><addtitle>Semin Immunopathol</addtitle><description>Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease but also key drivers of APS pathophysiology. Thrombotic events in APS can be attributed to various conspirators including activated endothelial cells, platelets, and myeloid-lineage cells, as well as derangements in coagulation and fibrinolytic systems. Furthermore, recent work has especially highlighted the role of neutrophil extracellular traps (NETs) and the complement system in APS thrombosis. Beyond acute thrombosis, patients with APS can also develop an occlusive vasculopathy, a long-term consequence of APS characterized by cell proliferation and infiltration that progressively expands the intima and leads to organ damage. This review will highlight known pathogenic factors in APS and will also briefly discuss similarities between APS and the thrombophilic coagulopathy of COVID-19.</description><subject>Antibodies, Antiphospholipid</subject><subject>Antiphospholipid antibodies</subject><subject>Antiphospholipid syndrome</subject><subject>Antiphospholipid Syndrome - complications</subject><subject>Antiphospholipid Syndrome - diagnosis</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell proliferation</subject><subject>Complement activation</subject><subject>COVID-19</subject><subject>COVID-19 - complications</subject><subject>Endothelial Cells</subject><subject>Fibrin</subject><subject>Humans</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Leukocytes (neutrophilic)</subject><subject>Pathology</subject><subject>Phospholipids</subject><subject>Review</subject><subject>Thromboinflammation</subject><subject>Thrombophilia</subject><subject>Thrombosis</subject><subject>Thrombosis - complications</subject><subject>Vascular Diseases</subject><issn>1863-2297</issn><issn>1863-2300</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9P3DAQxa2qqPxpv0APVaReegmM7ThxLpUqRAFpERc4W3biEKPETj0JaL89hl22pQcO1lie33ue0SPkK4VjClCdIACTNAfGcoCalvnjB3JAZclzxgE-vt5ZXe2TQ8R7AFFxUX0i-1xQxigtD8jqyja99g5HzEKXuXFcfJj7GEYT0GGmfZs9aGyWIUx67teZ8-ltdlMfMJ3BTa7NcO3bpLCfyV6nB7RftvWI3P4-uzm9yFfX55env1Z5U1TFnAvoCgGV1bazEsBwLcpC1LZpwRjDGWUFB12CaZnVIKvKdIKBlpLVhgpb8CPyc-M7LWa0bWP9HPWgpuhGHdcqaKfedrzr1V14UFLSklNIBj-2BjH8WSzOanTY2GHQ3oYFFStZCVTwgiX0-3_ofViiT-slSshaCip5otiGamJAjLbbDUNBPYelNmGpFJZ6CUs9JtG3f9fYSV7TSQDfAJha_s7Gv3-_Y_sEGkWh6w</recordid><startdate>20220501</startdate><enddate>20220501</enddate><creator>Knight, Jason S.</creator><creator>Kanthi, Yogendra</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20220501</creationdate><title>Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome</title><author>Knight, Jason S. ; Kanthi, Yogendra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-50f4507eaefe800b3a56459ecd0bbb3212430a60bd2ea0877bf520a8829b15e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antibodies, Antiphospholipid</topic><topic>Antiphospholipid antibodies</topic><topic>Antiphospholipid syndrome</topic><topic>Antiphospholipid Syndrome - complications</topic><topic>Antiphospholipid Syndrome - diagnosis</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell proliferation</topic><topic>Complement activation</topic><topic>COVID-19</topic><topic>COVID-19 - complications</topic><topic>Endothelial Cells</topic><topic>Fibrin</topic><topic>Humans</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Leukocytes (neutrophilic)</topic><topic>Pathology</topic><topic>Phospholipids</topic><topic>Review</topic><topic>Thromboinflammation</topic><topic>Thrombophilia</topic><topic>Thrombosis</topic><topic>Thrombosis - complications</topic><topic>Vascular Diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Knight, Jason S.</creatorcontrib><creatorcontrib>Kanthi, Yogendra</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Seminars in immunopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knight, Jason S.</au><au>Kanthi, Yogendra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome</atitle><jtitle>Seminars in immunopathology</jtitle><stitle>Semin Immunopathol</stitle><addtitle>Semin Immunopathol</addtitle><date>2022-05-01</date><risdate>2022</risdate><volume>44</volume><issue>3</issue><spage>347</spage><epage>362</epage><pages>347-362</pages><issn>1863-2297</issn><eissn>1863-2300</eissn><abstract>Antiphospholipid syndrome (APS) is an autoimmune thrombophilia propelled by circulating antiphospholipid antibodies that herald vascular thrombosis and obstetrical complications. Antiphospholipid antibodies recognize phospholipids and phospholipid-binding proteins and are not only markers of disease but also key drivers of APS pathophysiology. Thrombotic events in APS can be attributed to various conspirators including activated endothelial cells, platelets, and myeloid-lineage cells, as well as derangements in coagulation and fibrinolytic systems. Furthermore, recent work has especially highlighted the role of neutrophil extracellular traps (NETs) and the complement system in APS thrombosis. Beyond acute thrombosis, patients with APS can also develop an occlusive vasculopathy, a long-term consequence of APS characterized by cell proliferation and infiltration that progressively expands the intima and leads to organ damage. This review will highlight known pathogenic factors in APS and will also briefly discuss similarities between APS and the thrombophilic coagulopathy of COVID-19.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35122116</pmid><doi>10.1007/s00281-022-00916-w</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1863-2297 |
| ispartof | Seminars in immunopathology, 2022-05, Vol.44 (3), p.347-362 |
| issn | 1863-2297 1863-2300 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8816310 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Antibodies, Antiphospholipid Antiphospholipid antibodies Antiphospholipid syndrome Antiphospholipid Syndrome - complications Antiphospholipid Syndrome - diagnosis Autoimmune diseases Biomedical and Life Sciences Biomedicine Cell proliferation Complement activation COVID-19 COVID-19 - complications Endothelial Cells Fibrin Humans Immunology Internal Medicine Leukocytes (neutrophilic) Pathology Phospholipids Review Thromboinflammation Thrombophilia Thrombosis Thrombosis - complications Vascular Diseases |
| title | Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T13%3A03%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mechanisms%20of%20immunothrombosis%20and%20vasculopathy%20in%20antiphospholipid%20syndrome&rft.jtitle=Seminars%20in%20immunopathology&rft.au=Knight,%20Jason%20S.&rft.date=2022-05-01&rft.volume=44&rft.issue=3&rft.spage=347&rft.epage=362&rft.pages=347-362&rft.issn=1863-2297&rft.eissn=1863-2300&rft_id=info:doi/10.1007/s00281-022-00916-w&rft_dat=%3Cproquest_pubme%3E2626015342%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2658985183&rft_id=info:pmid/35122116&rfr_iscdi=true |