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Spontaneous Downregulation of Antibody/Autoantibody Synthesis in Susceptible Mice upon Chronic Exposure to Mercuric Chloride is not Owing to a General Immunosuppression
Author(s) -
Roether S.,
Rabbani H.,
Mellstedt H.,
AbediValugerdi M.
Publication year - 2002
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2002.01085.x
Subject(s) - antibody , autoantibody , autoimmunity , immune system , polyclonal antibodies , immunosuppression , immunology , autoimmune disease , immune complex , immunoglobulin e , chemistry , biology
Administration of mercuric chloride into susceptible rats and mice induces a systemic autoimmune disease, which is characterized by a T‐cell‐dependent polyclonal B‐cell activation, an increase in serum levels of immunoglobulin (Ig)G1 and IgE, production of antibodies of different specificities and development of renal IgG deposits. A peculiar feature of mercury‐induced autoimmunity is that the polyclonal B‐cell activation spontaneously disappears in spite of continuous injection of mercury. The exact mechanism(s) for autoregulation of mercury‐induced autoimmunity is not well understood. In the present study, we analysed the regulation of mercury‐induced immune/autoimmune responses in mice and tested whether spontaneous downregulation of these responses is owing to a general immunosuppression. Mercury‐susceptible [SJL (H‐2 s )] and ‐resistant [DBA/2 (H‐2 d )] mice were injected with mercury for 4, 10, 15 and 17 weeks. Immune/autoimmune responses were monitored in these mice. Thereafter, mercury‐injected mice for 17 weeks were further immunized with horse red blood cells (HRBC) to study whether the subsequent humoral immune response to a foreign antigen is suppressed. We found that except for IgG1 anti‐nucleolar antibody production and renal IgG1 deposition, other characteristics of mercury‐induced autoimmunity were downregulated in SJL (H‐2 s ) mice after chronic treatment with mercury. However, these mice did not show any reduction in the number of splenic antibody‐secreting cells and/or in serum titres of specific IgM, IgG1 and IgG2a anti‐HRBC antibodies in response to HRBC as compared with naïve mice. Similarly, in mercury‐resistant DBA/2 (H‐2 d ) mice, chronic treatment with mercury did not either suppress specific antibody responses against HRBC. Our findings show that the autoregulation of mercury‐induced immune/autoimmune responses observed after chronic treatment with mercury is not owing to a general immunosuppression.