ABSTRACT
Autoimmune thrombocytopenic purpura (ATP) is a bleeding disorder caused by excessive destruction of antibody-coated platelets. It is known that platelet destruction takes place in macrophages of reticulo-endothelial system, but immunological mechanisms involved in such destruction are unknown. The objective of this article is to review the literature concerning pathogenesis of ATP: to have controlled experimental conditions some animal laboratory models have been used. The (NZW X BXSB) F1 mice have been studied as autoimmune disease model and Harrington mouse as an immune purpura model. Studies in humans suggest that there are some differences in pathogenesis of acute or chronic ATP, particularly in reactive T cells. For example, in chronic form there are high levels of The (CD4+) activity concomitant with low levels of T suppressor (CD8+) activity, while in acute form there is no dominance of any particular T cell activity or CD4+ is even decreased. Mitogen lymphocyte proliferation is increased in chronic ATP but decreased in acute form.