| First Author | Yang H | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 3 | Pages | 1729-37 |
| PubMed ID | 15661938 | Mgi Jnum | J:96401 |
| Mgi Id | MGI:3530398 | Doi | 10.4049/jimmunol.174.3.1729 |
| Citation | Yang H, et al. (2005) Cathepsin S is required for murine autoimmune myasthenia gravis pathogenesis. J Immunol 174(3):1729-37 |
| abstractText | 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-gamma 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. |
