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We have previously hypothesized that mercury confers more adverse immunological effects on those mouse strains, which are genetically prone to develop spontaneous autoimmune diseases than on normal strains. In this study, we tested our hypothesis in tight skin 1 (Tsk1\/+) mice, a murine model for human scleroderma. As a support for our hypothesis, we observed that in Tsk1\/+ mice, B cells were spontaneously hyperactive and that treatment with mercury induced a strong immune\/autoimmune response in these mice, but not in their non\u2010Tsk (+\/+) littermates. This response was characterized by the formation of high numbers of splenic IgG1, IgG2b and IgG3 antibody\u2010secreting cells, increased serum levels of IgE, production of IgG1 antibodies against single\u2010stranded DNA (ssDNA), trinitrophenol (TNP) as well as thyroglobulin and the development of renal IgG1 deposits. Neither Tsk1\/+ mice nor F1 hybrid crosses between this strain, and mercury susceptible B10.S (H\u20102<jats:sup>s<\/jats:sup>) were able to produce IgG1\u2010ANolA in response to mercury. Moreover, mercury\u2010induced immune activation in Tsk1\/+ was not able to potentiate the progression of skin fibrosis in this strain. Thus, exposure to mercury accelerates the immune dysregulation, but not the development of skin fibrosis in Tsk1\/+ mice.<\/jats:p>","DOI":"10.1111\/j.0300-9475.2004.01415.x","type":"journal-article","created":{"date-parts":[[2004,5,6]],"date-time":"2004-05-06T14:53:32Z","timestamp":1083855212000},"page":"469-477","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Mercuric Chloride Induces a Strong Immune Activation, but does not Accelerate the Development of Dermal Fibrosis in Tight Skin 1 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