HgC12 induces T and B cells to proliferate and differentiate in BN rats.

Mercuric chloride induces in Brown-Norway (BN) rats an autoimmune disease characterized by the production of various autoantibodies and by a marked increase in the IgE serum concentration. This agent is responsible for a T dependent polyclonal activation of B cells, which is probably due to the emergence of autoreactive T cells. The aim of this study was to evaluate the effect of HgCl2 injections on lymphoid organs and on the serum concentration of the various Ig isotypes. HgCl2 induced (1) a lymphoproliferation in spleen and lymph nodes involving B and T helper cells while the number of T suppressor/cytotoxic cells was not modified, (2) an increase in the number of Ig containing cells resulting in a rise in all serum Ig isotypes, and (3) an early thymic atrophy probably immunologically mediated, which was not involved in the induction phase of the disease since adult thymectomy had no effect. These findings demonstrate that the polyclonal effect of HgCl2 is not isotype-restricted although the IgE response is predominantly affected and they support evidence for a major role for an excess of T help in the HgCl2-induced polyclonal activation of B cells. It was also observed that B cell areas are present in normal BN rat thymuses, the potential role of which in the induction of autoimmunity remains to be investigated.