Cathepsin S is required for murine autoimmune myasthenia gravis pathogenesis

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

Research output: Contribution to journalArticle

51 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1729-1737
Number of pages9
JournalJournal of Immunology
Volume174
Issue number3
DOIs
StatePublished - Feb 1 2005

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Yang, H., Kala, M., Scott, B. G., Goluszko, E., Chapman, H. A., & Christadoss, P. (2005). Cathepsin S is required for murine autoimmune myasthenia gravis pathogenesis. Journal of Immunology, 174(3), 1729-1737. https://doi.org/10.4049/jimmunol.174.3.1729