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TOXICOLOGICAL SCIENCES, 142(2), 2014, 339?doi: 10.1093/toxsci/kfu189 Advance Access Publication Date: September 18,Cathepsin B Regulates the Look and Severity of Mercury-Induced Inflammation and AutoimmunityChristopher B. Toomey, David M. Cauvi, John C. Hamel, Andrea E. Ramirez, and K. Michael Pollard,Department of Ophthalmology, College of Medicine, Duke University, 2351 Erwin Road, Durham, North Carolina 27710, Division of Surgery and Center for Investigations of Well being and Education Disparities, School of Medicine, University of California, San Diego, 9500 Gilman Drive, No. 0739, La Jolla, California 92093-0739 and Division of Molecular and Adiponectin/Acrp30 Protein Gene ID Experimental Medicine, The Scripps Study Institute, 10550 North Torrey Pines Road, La Jolla, CaliforniaTo whom correspondence ought to be addressed at Division of Molecular and Experimental Medicine MEM125, The Scripps Analysis Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. Fax: (858) 784-8836. VEGF165 Protein custom synthesis E-mail: [email protected] and resistance to systemic autoimmunity are genetically regulated. This really is especially true for murine mercury-induced autoimmunity (mHgIA) exactly where DBA/2J mice are deemed resistant to illness including polyclonal B cell activation, autoantibody responses, and immune complex deposits. To recognize feasible mechanisms for the resistance to mHgIA, we exposed mHgIA sensitive B10.S and resistant DBA/2J mice to HgCl2 and assessed inflammation and pro-inflammatory responses at the site of exposure and subsequent improvement of markers of systemic autoimmunity. DBA/2J mice showed small evidence of induration at the internet site of exposure, expression of proinflammatory cytokines, T cell activation, or autoantibody production, though they did exhibit enhanced levels of total serum IgG and IgG1. In contrast B10.S mice developed important inflammation collectively with enhanced expression of inflammasome component NLRP3, proinflammatory cytokines IL-1b, TNF-a, and IFN-c, hypergammaglobulinemia, splenomegaly, CD4?T-cell activation, and production of autoantibodies. Inflammation in B10.S mice was associated having a selective raise in activity of cysteine cathepsin B but not cathepsins L or S. Enhanced cathepsin B activity was not dependent on cytokines required for mHgIA but treatment with CA-074, a cathepsin B inhibitor, led to transient reduction of local induration, expression of inflammatory cytokines, and subsequent attenuation with the systemic adaptive.