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- W1988334989 abstract "Modified forms of LDL are immunogenic and activate both cell-mediated and humoral immune responses. Both types of responses are pro-inflammatory and are probably primary players in the perpetuation of the chronic inflammatory reaction characteristic of atherosclerosis. The immunologic response to modified LDL can be directed to MHC-II-associated peptides in the case of T helper cells, and to a variety of epitopes-modified lysine groups, modified phospholipids, proteins that become associated with oxidized LDL (such as beta2GP1)--in the case of B cell responses. T cell activation is likely to play a major role through cross-activation of macrophages. Humoral responses to modified LDL are pathogenic as a consequence of the formation of antigen-antibody complexes containing modified LDL and IgG antibodies. Those immune complexes induce cholesterol ester accumulation in macrophages and macrophage-like cells, and induce the release of pro-inflammatory cytokines, chemokines, oxygen active radicals, and matrix metalloproteinases from those cells. There is no conclusive evidence supporting a protective role for IgM antibodies in humans, possibly because autoantibodies to modified lipoproteins are predominantly of the IgG isotype." @default.
- W1988334989 created "2016-06-24" @default.
- W1988334989 creator A5019136419 @default.
- W1988334989 creator A5046063952 @default.
- W1988334989 date "2008-10-01" @default.
- W1988334989 modified "2023-10-16" @default.
- W1988334989 title "Atherogenesis and the humoral immune response to modified lipoproteins" @default.
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- W1988334989 doi "https://doi.org/10.1016/j.atherosclerosis.2008.03.025" @default.
- W1988334989 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2605965" @default.
- W1988334989 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18513726" @default.