Abstract
Natural IgM class antibody constitutes a protective factor offsetting the proatherogenic effects and cellular toxicity of oxidized low-density lipoproteins (LDL). The protective, antiatherogenic action of IgM class antibody takes place at two levels.
The first, and the more important of both, is so called competitive inhibition. Binding of IgM class antibody to oxidized LDL results in reducing their phagocytosis by macrophages or vascular wall smooth muscle cells.
The result is decreased formation of the foam cell as the basic substrate of the atherogenic process. Another, possibly only a complementary mechanism, is the formation of immune complexes among IgM class antibody and oxLDL.
These immune complexes are removed from the circulation to the liver or the spleen where they are eventually disposed of. Foam cell formation is again reduced.
In acute coronary syndrome patients, IgM class antibody is involved in the stabilization of vulnerable plaques and in repair of injured tissue.