Immunopathogenesis of atherosclerosis
Recent clinical studies indicate that the number of microbial infections (the “pathogen burden”) critically determines the development and progression of atherosclerotic disease. Viruses or bacteria with a specific tropism for cells of the vascular wall may contribute to the initial vascular injury...
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Veröffentlicht in: | Journal of leukocyte biology 2004-08, Vol.76 (2), p.300-306 |
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container_title | Journal of leukocyte biology |
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creator | Ludewig, Burkhard Krebs, Philippe Scandella, Elke |
description | Recent clinical studies indicate that the number of microbial infections (the “pathogen burden”) critically determines the development and progression of atherosclerotic disease. Viruses or bacteria with a specific tropism for cells of the vascular wall may contribute to the initial vascular injury via direct cytopathic effects or via the induction of genuine autoimmune responses. Immunopathological processes such as molecular mimicry, epitope spreading, or bystander activation of self‐reactive lymphocytes most likely fuel the chronic inflammatory process in the vascular wall. Recognition of atherogenesis as a pathogen‐driven, immunopathological process makes this disease amenable to new treatment strategies such as vaccination or immunomodulation. |
doi_str_mv | 10.1189/jlb.1203605 |
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Recognition of atherogenesis as a pathogen‐driven, immunopathological process makes this disease amenable to new treatment strategies such as vaccination or immunomodulation.</description><subject>Animals</subject><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - immunology</subject><subject>Arteriosclerosis - physiopathology</subject><subject>bystander activation</subject><subject>Cardiovascular System - immunology</subject><subject>Cardiovascular System - microbiology</subject><subject>Communicable Diseases - complications</subject><subject>Communicable Diseases - immunology</subject><subject>Communicable Diseases - physiopathology</subject><subject>Epitopes - immunology</subject><subject>Humans</subject><subject>immunopathology</subject><subject>Inflammation - etiology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - microbiology</subject><subject>Inflammation - physiopathology</subject><subject>molecular mimicry</subject><subject>Molecular Mimicry - immunology</subject><subject>transgenic mouse model</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAQhi0EoqUwsaMusKCU80dsZ4SKj6JKLDBbju20qZymxI2i_ntcJRIbLHc66bn3dA9C1xhmGMvsYePzGSZAOaQnaIwzKhPKBT1FYxAMJykDGKGLEDYAQAmHczTCKdCMcTlGt4uqarf1Tu_X9cptXSjDtC6mcXRNHYw_1jJcorNC--Cuhj5BXy_Pn_O3ZPnxupg_LhPDMIckNQXLUw1MQMYyIjOjATPhdIGtsxmxxkhjrcm5pVIWmmKOTU4t2JQWlGo6QXd97q6pv1sX9qoqg3He662r26A4FxyIJP-CWAhgwGQE73vQxEdC4wq1a8pKNweFQR31qahPDfoifTPEtnnl7C87-IoA9EBXenf4K0u9L5-ARuMTdNuvrMvVuisbp0KlvY8XiOq6TnBF1JH7Aexzhk4</recordid><startdate>200408</startdate><enddate>200408</enddate><creator>Ludewig, Burkhard</creator><creator>Krebs, Philippe</creator><creator>Scandella, Elke</creator><general>Society for Leukocyte Biology</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>200408</creationdate><title>Immunopathogenesis of atherosclerosis</title><author>Ludewig, Burkhard ; Krebs, Philippe ; Scandella, Elke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4160-5cf4b5a0470949289ca0147eaf1ded92dcc8cddcb6d388fa3161cb3d0d53f33a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Arteriosclerosis - etiology</topic><topic>Arteriosclerosis - immunology</topic><topic>Arteriosclerosis - physiopathology</topic><topic>bystander activation</topic><topic>Cardiovascular System - immunology</topic><topic>Cardiovascular System - microbiology</topic><topic>Communicable Diseases - complications</topic><topic>Communicable Diseases - immunology</topic><topic>Communicable Diseases - physiopathology</topic><topic>Epitopes - immunology</topic><topic>Humans</topic><topic>immunopathology</topic><topic>Inflammation - etiology</topic><topic>Inflammation - immunology</topic><topic>Inflammation - microbiology</topic><topic>Inflammation - physiopathology</topic><topic>molecular mimicry</topic><topic>Molecular Mimicry - immunology</topic><topic>transgenic mouse model</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ludewig, Burkhard</creatorcontrib><creatorcontrib>Krebs, Philippe</creatorcontrib><creatorcontrib>Scandella, Elke</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>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ludewig, Burkhard</au><au>Krebs, Philippe</au><au>Scandella, Elke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunopathogenesis of atherosclerosis</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2004-08</date><risdate>2004</risdate><volume>76</volume><issue>2</issue><spage>300</spage><epage>306</epage><pages>300-306</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>Recent clinical studies indicate that the number of microbial infections (the “pathogen burden”) critically determines the development and progression of atherosclerotic disease. 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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Animals Arteriosclerosis - etiology Arteriosclerosis - immunology Arteriosclerosis - physiopathology bystander activation Cardiovascular System - immunology Cardiovascular System - microbiology Communicable Diseases - complications Communicable Diseases - immunology Communicable Diseases - physiopathology Epitopes - immunology Humans immunopathology Inflammation - etiology Inflammation - immunology Inflammation - microbiology Inflammation - physiopathology molecular mimicry Molecular Mimicry - immunology transgenic mouse model |
title | Immunopathogenesis of atherosclerosis |
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