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Macrophages lesions starting with

The first inflammatory stage of atherosclerosis starts early in life with more severe lesions developing only if classical risk factors, especially cholesterol, remain present. Immune responses mounted against antigens cross-react with homologous host proteins in a form of molecular mimicry, for example, HSP are secreted by C. pneumoniae, H. pylori, mammalian vascular cells exposed to stress such as CVD risk factors, and cells within atherosclerotic plaques In addition, serum titers of anti-HSP antibodies are correlated positively with the future risk of CHD, and purified anti-HSP antibodies lyse stressed human EC and macrophages in vitro. Furthermore, immunization with HSP exacerbate athersclerosis in animal models (reviewed in refs. 212,213). However, there is molecular mimicry between epitopes of oxLDL and Streptococcus pneumonia in LDLR -/- mice pneumococcal immunization led to increased IgM levels against oxLDL and decreased the extent of atherosclerosis (214). [Pg.118]


See other pages where Macrophages lesions starting with is mentioned: [Pg.437]    [Pg.392]    [Pg.418]    [Pg.2031]    [Pg.264]    [Pg.274]    [Pg.149]    [Pg.88]    [Pg.35]    [Pg.224]   
See also in sourсe #XX -- [ Pg.225 ]




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