期刊
AMERICAN JOURNAL OF THE MEDICAL SCIENCES
卷 327, 期 4, 页码 212-216出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00000441-200404000-00007
关键词
arthritis; collagen; peptide; immunotherapy; autoimmunity
资金
- NIAMS NIH HHS [AR-43589, AR-39166] Funding Source: Medline
The authors undertook the identification of peptides capable of altering the immune response to type II collagen (CII) in the context of HLA-DR, as suppressing the immune response to CII could clarify the role of CII autoimmunity in the pathogenesis of disease. To produce synthetic peptides with the potential of disrupting the DR1-restricted immune response, synthetic analog peptides were developed that contain sitedirected substitutions in critical positions. When these analog peptides were used to treat collagen-induced arthritis in DR1 transgenic mice, an analog peptide, CII 256-276 (N-263, D-266), was identified that inhibited T-cell responses in vitro. The data from studies with this analog peptide establish that CII 256-276 (N-236, D-266) a potent suppressor of the DR-mediated immune response to CII and that its effect is mediated, at least in part, by interleukin-4. An analog peptide of CII recognized by T cells in the context of a human major histocompatibility complex molecule should have therapeutic significance for autoimmune arthritis.
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