Increased expression of class II major histocompatibility complex molecules on B cells in rats susceptible or resistant to HgC12-induced autoimmunity

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Abstract
Administration of HgCl2 to the susceptible Brown-Norway (BN)rais induces an autoimmune disease characterized by a T-dependent polyclonal activation of B cells responsible for a dramatic increase in serum IgE concentration. The resistant Lewis (LEW) rats injected with HgCi2. do not exhibit such autoimmune manifestations. We show here that, upon HgCl2 injections, major histocompalibility complex (MHC) class II molecule expression is increased very early in lymph nodes and spleen B cells from both strains. So far. it is the earliest marker (day 3)of the effect of HgCI2on the immune system. In both strains this enhancement is transient, but regulatory mechanisms arc much more efficient in the resistant LEW strain than in the susceptible BN strain, In addition, we observed that MHC class II molecule expression on B cells differs according to the organ and the rat strain tested. All these findings are discussed in an attempt to underline the role of MHC class II molecule expression in the occurrence of mercury-induced stutoimmunity.