Atherogenesis and the humoral immune response to modified lipoproteins.

摘要: Modified forms of LDL are immunogenic and activate both cell-mediated humoral immune responses. Both types responses pro-inflammatory probably primary players in the perpetuation chronic inflammatory reaction characteristic atherosclerosis. The immunologic response to modified can be directed MHC-II-associated peptides case T helper cells, a variety epitopes-modified lysine groups, phospholipids, proteins that become associated with oxidized (such as beta2GP1)--in B cell activation is likely play major role through cross-activation macrophages. Humoral pathogenic consequence formation antigen-antibody complexes containing IgG antibodies. Those induce cholesterol ester accumulation macrophages macrophage-like release cytokines, chemokines, oxygen active radicals, matrix metalloproteinases from those cells. There no conclusive evidence supporting protective for IgM antibodies humans, possibly because autoantibodies lipoproteins predominantly isotype.