Platelets, immune complex aggregation

M29. Myllyla, G., Aggregation of human blood platelets by immune complexes in the sedimentation pattern test. Scand. J. Haematol. Suppl. 19, 1-50 (1973). 

Liischer, E. F., Immune Complexes and Platelet Aggregation, Acta Med. 

Platelet aggregation may occur as a result of immune-complex formation, resulting in the formation of microthrombi and the release of vasoactive mediators. Also, insoluble complexes may be phagocy-tized by macrophages and activate these cells. 

The mechanism of action of the immunological and anti-inflammatory effects of antimalarials include inhibition of phospholipase A, inhibition of platelet aggregation, a range of lysosomal effects (e.g., an increase in pH, membrane stabilization, and inhibition of release and activity of lysosomal enzymes), inhibition of phagocytosis, an increase in intracellular pH in cytoplasmic vacuoles leading to decreased stimulation of autoimmune CD4 T cells, decreased cytokine release from lymphocytes and stimulated monocytes, inhibition of immune complex formation, and antioxidant activity. In patients with porphyria cutanea tarda, chloroquine and hydroxychloroquine bind to porphyrins and/or iron to facilitate their hepatic clearance. The ability to bind to melanin and other pigments may contribute to the retinal toxicity seen occasionally when anti-malarial agents are used. 

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