| pubmed-article:18600328 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0678815 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0039198 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C2936411 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0971858 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:18600328 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:18600328 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18600328 | pubmed:dateCreated | 2008-9-30 | lld:pubmed |
| pubmed-article:18600328 | pubmed:abstractText | Rheumatoid arthritis (RA) is a systemic autoimmune disease mediated by T cells. Collagen type II (CII) is one of the autoantigens associated with RA. CII263-272 is a predominant CII antigenic peptide that can induce T-cell activation upon binding to MHC and interaction with the appropriate T-cell receptor (TCR). Altered CII263-272 peptides with substitution of specific amino acids could bind to RA-associated HLA-DR4/1 with no T cell stimulating effects and could inhibit T cell activation in RA. We performed this study to evaluate the effect of mucosal administration and to explore the mechanism of the inhibitory effect of altered CII263-272 peptide (267Q-->A, 270K-->A and 271G-->A) on collagen induced arthritis (CIA). CIA was induced in Lewis rats by immunization with bovine CII. Altered CII263-272 peptide was given intranasally beginning from arthritis onset. Wild CII263-272 peptide or PBS was administered as controls. Therapeutic effects were evaluated by arthritis scores, body weight change, and joint pathologic scores. The anti-CII antibody and its subtypes and the cytokines, IFN-gamma, IL-10, and IL-17 were measured with ELISA. Foxp3+CD4+CD25+ regulatory T cell induction was assessed by FACS analysis. Following treatment with the altered CII263-272 peptide, arthiritis scores were reduced and body weight was increased. The altered CII263-272 peptide could retard the histologic lesion of the joints. The titers of anti-CII antibodies IgG2a in altered CII263-272 peptide treated rats decreased markedly compared to PBS-treated rats. The serum levels of IFN-gamma in rats treated with altered peptide was lower than that of rats treated with wild CII263-272 peptide and PBS. No differences were observed in the levels of serum IL-10 among the three groups. The altered CII263-272 peptide could decrease serum level of IL-17 and increase peripheral Foxp3+CD4+CD25+ T cells at early stage of CIA. Mucosal administration of altered CII263-272 peptide could effectively inhibit the progression of CIA. Altered CII263-272 peptide could suppress Th17 cells and expand regulatory T cells in the early stage of the disease. The IgG2a subtype of anti-CII antibodies and IFN-gamma were reduced and in vivo Th1 responses were inhibited as a result of altered CII peptide treatment. Altered CII peptide is likely therapeutic in RA. | lld:pubmed |
| pubmed-article:18600328 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18600328 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18600328 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18600328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18600328 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18600328 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18600328 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:18600328 | pubmed:issn | 0172-8172 | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:HausE MEM | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:MORAPP | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:RAJR SRS | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:LiZhanguoZ | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:ZhaoJinxiaJ | lld:pubmed |
| pubmed-article:18600328 | pubmed:author | pubmed-author:ShiJinxiaJ | lld:pubmed |
| pubmed-article:18600328 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18600328 | pubmed:volume | 29 | lld:pubmed |
| pubmed-article:18600328 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18600328 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18600328 | pubmed:pagination | 9-16 | lld:pubmed |
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| pubmed-article:18600328 | pubmed:meshHeading | pubmed-meshheading:18600328... | lld:pubmed |
| pubmed-article:18600328 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18600328 | pubmed:articleTitle | Mucosal administration of an altered CII263-272 peptide inhibits collagen-induced arthritis by suppression of Th1/Th17 cells and expansion of regulatory T cells. | lld:pubmed |
| pubmed-article:18600328 | pubmed:affiliation | Department of Rheumatology and Immunology, People's Hospital, Peking University Medical School, 11 Xizhimen South St., Beijing, 100044, China. zhao-jinxia@163.com | lld:pubmed |
| pubmed-article:18600328 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18600328 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
