期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 3, 页码 1729-1737出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.3.1729
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- NHLBI NIH HHS [HL48621] Funding Source: Medline
- NIAID NIH HHS [R21AI049995] Funding Source: Medline
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 Nitro IFN-gamma production by lymph node cells front 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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