IMMUNOREGULATION AND ANTI-NUCLEAR ANTIBODIES IN MERCURY-INDUCED GLOMERULOPATHY IN THE RAT

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 45  (1) , 64-71
Abstract
Pathogenesis of drug-induced autoimmune antibodies is in most cases uncertain. The recent demonstration of T cell aberrations in human and experimental drug-induced autoimmune disease suggested that immunodysregulation might form the basis of an uncontrolled B cell autoreactivity leading to autoantibody production. Lymphocytic stimulation by phytohemagglutinin (PHA) and concanvalin A-activated suppressor cell activity was measured in an experimental model of Hg-induced immune complex glomerulopathy associated with anti-nuclear antibodies and vasculitis in PVG/c rats. General T cell reactivity to PHA and concanavalin A-activated suppressor function as measured by a syngeneic target cell assay was significantly decreased in Hg-diseased rats, compared with saline-injected controls. The effect of neonatal and adult thymectomy on the course of Hg-induced disease was studied. Anti-nuclear antibody activity and glomerular immune aggregate formation were accelerated by neonatal thymectomy. Thymectomy at adult age had no significant effect on the interval between the start of Hg administration and the appearance of serological and renal abnormalities. Hg affected effector and regulatory T cell functions and immunodysregulation was of pathogenetic significance in this model of drug-induced disease.