Mechanisms of autoantibody-mediated thrombosis
It is widely hypothesized that autoantibodies directly contribute to the prothrombotic state in the antiphospholipid syndrome (APS). The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more...
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| Veröffentlicht in: | Lupus 1998-01, Vol.7 (2_suppl), p.114-119 |
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| creator | Roubey, R.A.S. |
| description | It is widely hypothesized that autoantibodies directly contribute to the prothrombotic state in the antiphospholipid syndrome (APS). The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more precise investigation of the interactions of autoantibodies and antigens, and the effects of these interaction on hemostastis. Recent studies suggest that two types of interactions may be important in the pathophysiology of APS: (1) antibody cross-linking of membrane bound antigens may alter the kinetics of phospholipid-dependent reactions; and (2) antibody cross-linking of antigens bound to cell surface receptors may trigger signal transduction and cellular activation. In light of these findings, previous reports implicating various mechanisms of autoantibody-mediated thrombosis are being re-evaluated. |
| doi_str_mv | 10.1177/096120339800700226 |
| format | Article |
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The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more precise investigation of the interactions of autoantibodies and antigens, and the effects of these interaction on hemostastis. Recent studies suggest that two types of interactions may be important in the pathophysiology of APS: (1) antibody cross-linking of membrane bound antigens may alter the kinetics of phospholipid-dependent reactions; and (2) antibody cross-linking of antigens bound to cell surface receptors may trigger signal transduction and cellular activation. 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The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more precise investigation of the interactions of autoantibodies and antigens, and the effects of these interaction on hemostastis. Recent studies suggest that two types of interactions may be important in the pathophysiology of APS: (1) antibody cross-linking of membrane bound antigens may alter the kinetics of phospholipid-dependent reactions; and (2) antibody cross-linking of antigens bound to cell surface receptors may trigger signal transduction and cellular activation. In light of these findings, previous reports implicating various mechanisms of autoantibody-mediated thrombosis are being re-evaluated.</description><subject>Antibodies, Anticardiolipin - immunology</subject><subject>Antigen-Antibody Reactions</subject><subject>Antiphospholipid Syndrome - immunology</subject><subject>Autoantibodies - immunology</subject><subject>Autoantigens - immunology</subject><subject>Autoimmune Diseases - immunology</subject><subject>beta 2-Glycoprotein I</subject><subject>Cell Adhesion</subject><subject>Epitopes - immunology</subject><subject>Glycoproteins - immunology</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>Lupus Coagulation Inhibitor - immunology</subject><subject>Membrane Lipids - immunology</subject><subject>Models, Immunological</subject><subject>Monocytes - metabolism</subject><subject>Phospholipids - immunology</subject><subject>Plasminogen Activator Inhibitor 1 - metabolism</subject><subject>Thrombophilia - immunology</subject><subject>Thromboplastin - physiology</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - immunology</subject><issn>0961-2033</issn><issn>1477-0962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkLtOwzAUhi0EKqXwAkhIndhCfYsvI6q4SUUsMFu2c0JTNXGxk6Fvj6NWLEgwefi_8_ucD6Frgu8IkXKBtSAUM6YVxhJjSsUJmhIuZZETeoqmI1CMxDm6SGmDMWZEiwmaaEW4UHKK7l7Br23XpDbNQz23Qx9s1zcuVPuihaqxPVTzfh1D60Jq0iU6q-02wdXxnaGPx4f35XOxent6Wd6vCs9Z2Rd13qdyNWWQf8mrKOUJtVxTW7kSQGApLVZKY6-s1s67shICHAgmgFhashm6PfTuYvgaIPWmbZKH7dZ2EIZk8rWcl4L8CxKZDxV8BOkB9DGkFKE2u9i0Nu4NwWa0aX7bzEM3x_bBZRs_I0d9OV8c8mQ_wWzCELts5a_Gb1oBe48</recordid><startdate>19980101</startdate><enddate>19980101</enddate><creator>Roubey, R.A.S.</creator><general>SAGE Publications</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19980101</creationdate><title>Mechanisms of autoantibody-mediated thrombosis</title><author>Roubey, R.A.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-f007dbf23e46896288c12a492adb5ee6077a08890c8a99bcb5d66ebe636e1a253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Antibodies, Anticardiolipin - immunology</topic><topic>Antigen-Antibody Reactions</topic><topic>Antiphospholipid Syndrome - immunology</topic><topic>Autoantibodies - immunology</topic><topic>Autoantigens - immunology</topic><topic>Autoimmune Diseases - immunology</topic><topic>beta 2-Glycoprotein I</topic><topic>Cell Adhesion</topic><topic>Epitopes - immunology</topic><topic>Glycoproteins - immunology</topic><topic>Hemostasis</topic><topic>Humans</topic><topic>Lupus Coagulation Inhibitor - immunology</topic><topic>Membrane Lipids - immunology</topic><topic>Models, Immunological</topic><topic>Monocytes - metabolism</topic><topic>Phospholipids - immunology</topic><topic>Plasminogen Activator Inhibitor 1 - metabolism</topic><topic>Thrombophilia - immunology</topic><topic>Thromboplastin - physiology</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roubey, R.A.S.</creatorcontrib><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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Lupus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roubey, R.A.S.</au><au>Hughes, GRV</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of autoantibody-mediated thrombosis</atitle><jtitle>Lupus</jtitle><addtitle>Lupus</addtitle><date>1998-01-01</date><risdate>1998</risdate><volume>7</volume><issue>2_suppl</issue><spage>114</spage><epage>119</epage><pages>114-119</pages><issn>0961-2033</issn><eissn>1477-0962</eissn><abstract>It is widely hypothesized that autoantibodies directly contribute to the prothrombotic state in the antiphospholipid syndrome (APS). The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more precise investigation of the interactions of autoantibodies and antigens, and the effects of these interaction on hemostastis. Recent studies suggest that two types of interactions may be important in the pathophysiology of APS: (1) antibody cross-linking of membrane bound antigens may alter the kinetics of phospholipid-dependent reactions; and (2) antibody cross-linking of antigens bound to cell surface receptors may trigger signal transduction and cellular activation. In light of these findings, previous reports implicating various mechanisms of autoantibody-mediated thrombosis are being re-evaluated.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>9814687</pmid><doi>10.1177/096120339800700226</doi><tpages>6</tpages></addata></record> |
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| identifier | ISSN: 0961-2033 |
| ispartof | Lupus, 1998-01, Vol.7 (2_suppl), p.114-119 |
| issn | 0961-2033 1477-0962 |
| language | eng |
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| source | MEDLINE; SAGE Complete |
| subjects | Antibodies, Anticardiolipin - immunology Antigen-Antibody Reactions Antiphospholipid Syndrome - immunology Autoantibodies - immunology Autoantigens - immunology Autoimmune Diseases - immunology beta 2-Glycoprotein I Cell Adhesion Epitopes - immunology Glycoproteins - immunology Hemostasis Humans Lupus Coagulation Inhibitor - immunology Membrane Lipids - immunology Models, Immunological Monocytes - metabolism Phospholipids - immunology Plasminogen Activator Inhibitor 1 - metabolism Thrombophilia - immunology Thromboplastin - physiology Thrombosis - etiology Thrombosis - immunology |
| title | Mechanisms of autoantibody-mediated thrombosis |
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