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. Heavy 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 roles of T-helper (Th)1 and Th2 cells and their respective cytokines in the pathogenesis of mercury-induced disease. This article reviews recent studies that have examined the patterns of cytokine gene expression and where investigators have manipulated the Th1 and Th2 responses that occur during mercury-induced autoimmunity. Finally, we will discuss some biochemical/molecular mechanisms by which heavy metals may induce cytokine gene expression.
Bagenstose
L M
LM
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Salgame
P
P
Monestier
M
M
D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000235:genetics / Q000276:immunology; D015551:Autoimmunity / Q000187:drug effects* / Q000235:genetics; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008627:Mercuric Chloride / Q000633:toxicity*; D051379:Mice; D051381:Rats; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology
D016207:Cytokines; D008627:Mercuric Chloride