Cytokine regulation of a rodent model of mercuric chloride-induced autoimmunity

Experimental models of chemically induced autoimmunity have contributed to our understanding of the development of autoimmune diseases in humans. Heav y metals such as mercury induce a dramatic activation of the immune system and autoantibody production in genetically susceptible rats and mice. This autoimmune syndrome is dependent on T cells, which are important for B-cell activation and cytokine secretion. Several studies have focused on the rol es of T-helper (Th)1 and Th2 cells and their respective cytokines in the pa thogenesis of mercury-induced disease. This article reviews recent studies that have examined the patterns of cytokine gene expression and where inves tigators have manipulated the Th1 and Th2 responses that occur during mercu ry-induced autoimmunity. Finally, we will discuss some biochemical/molecula r mechanisms by which heavy metals may induce cytokine gene expression.