期刊
ATHEROSCLEROSIS
卷 200, 期 2, 页码 239-246出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2008.03.025
关键词
Atherosclerosis; Autoimmunity; LDL antibodies; Phospholipid antibodies; Immune complexes; Vascular inflammation
资金
- National Institutes of Health/NHLBI [PO1-HL55782]
- Juvenile Diabetes Research Foundation [1-2006-49]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL055782] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK081352] Funding Source: NIH RePORTER
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 beta 2GP1)-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. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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