ATTENTION: The software behind KU ScholarWorks is being upgraded to a new version. Starting July 15th, users will not be able to log in to the system, add items, nor make any changes until the new version is in place at the end of July. Searching for articles and opening files will continue to work while the system is being updated. If you have any questions, please contact Marianne Reed at mreed@ku.edu .

Show simple item record

dc.contributor.authorBuyuktimkin, Barlas
dc.contributor.authorKiptoo, Paul
dc.contributor.authorSiahaan, Teruna J.
dc.date.accessioned2015-09-25T14:04:06Z
dc.date.available2015-09-25T14:04:06Z
dc.date.issued2014-11
dc.identifier.citationBüyüktimkin B, Kiptoo P, Siahaan TJ (2014) Bifunctional Peptide Inhibitors Suppress Interleukin-6 Proliferation and Ameliorates Murine Collagen-Induced Arthritis. J Clin Cell Immunol 5: 273. doi:10.4172/2155-9899.1000273.en_US
dc.identifier.urihttp://hdl.handle.net/1808/18508
dc.descriptionThis is the published version. Copyright 2014 OMICS Internationalen_US
dc.description.abstractThe objective of this study is to evaluate the efficacy and potential mechanism of action of type-II collagen bifunctional peptide inhibitor (CII-BPI) molecules in suppressing rheumatoid arthritis in the collagen-induced arthritis (CIA) mouse model. CII-BPI molecules (CII-BPI-1, CII-BPI-2, and CII-BPI-3) were formed through conjugation between an antigenic peptide derived from type-II collagen and a cell adhesion peptide LABL (CD11a237-246) from the I-domain of LFA-1 via a linker molecule. The hypothesis is that the CII-BPI molecules simultaneously bind to MHC-II and ICAM-1 on the surface of APC and block maturation of the immunological synapse. As a result, the differentiation of naïve T cells is altered from inflammatory to regulatory and/or suppressor T cells. The efficacies of CII-BPI molecules were evaluated upon intravenous injections in CIA mice. Results showed that CII-BPI-1 and CIIBPI- 2 suppressed the joint inflammations in CIA mice in a dose-dependent manner and were more potent than the respective antigenic peptides alone. CII-BPI-3 was not as efficacious as CII-BPI-1 and CII-BPI-2. Significantly less joint damage was observed in CII-BPI-2 and CII-2 treated mice than in the control. The production of IL-6 was significantly lower at the peak of disease in mice treated with CII-BPI-2 compared to those treated with CII-2 and control. In conclusion, this is the first proof-of-concept study showing that BPI molecules can be used to suppress RA and may be a potential therapeutic strategy for the treatment of rheumatoid arthritis.en_US
dc.publisherOMICS Internationalen_US
dc.titleBifunctional Peptide Inhibitors Suppress Interleukin-6 Proliferation and Ameliorates Murine Collagen-Induced Arthritisen_US
dc.typeArticle
kusw.kuauthorBuyuktimkin, Barlas
kusw.kuauthorKiptoo, Paul
kusw.kuauthorSiahaan, Teruna J.
kusw.kudepartmentPharmaceutical Chemistryen_US
dc.identifier.doi10.4172/2155-9899.1000273
kusw.oaversionScholarly/refereed, publisher version
kusw.oapolicyThis item meets KU Open Access policy criteria.
dc.rights.accessrightsopenAccess


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record