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Cathepsin S Is Required for Murine Autoimmune Myasthenia Gravis Pathogenesis¹

Huan Yang^*, Mrinalini Kala, Benjamin G. Scott^*, Elzbieta Goluszko^*, Harold A. Chapman and Premkumar Christadoss^2,*

^* Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1070; and Department of Medicine and Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0130

Because presentation of acetylcholine receptor (AChR) peptides to T cells is critical to the development of myasthenia gravis, we examined the role of cathepsin S (Cat S) in experimental autoimmune myasthenia gravis (EAMG) induced by AChR immunization. Compared with wild type, Cat S null mice were markedly resistant to the development of EAMG, and showed reduced T and B cell responses to AChR. Cat S null mice immunized with immunodominant AChR peptides showed weak responses, indicating failed peptide presentation accounted for autoimmune resistance. A Cat S inhibitor suppressed in vitro IFN- production by lymph node cells from AChR-immunized, DR3-bearing transgenic mice. Because Cat S null mice are not severely immunocompromised, Cat S inhibitors could be tested for their therapeutic potential in EAMG.

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