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dc.contributor.authorManikwar, Prakash
dc.contributor.authorKiptoo, Paul
dc.contributor.authorBadawi, Ahmed H.
dc.contributor.authorBüyüktimkin, Barlas
dc.contributor.authorSiahaan, Teruna J.
dc.date.accessioned2017-06-22T15:46:38Z
dc.date.available2017-06-22T15:46:38Z
dc.date.issued2012-07
dc.identifier.citationManikwar, P., Kiptoo, P., Badawi, A. H., Büyüktimkin, B. and Siahaan, T. J. (2012), Antigen-specific blocking of CD4-Specific immunological synapse formation using BPI and current therapies for autoimmune diseases. Med Res Rev, 32: 727–764. doi:10.1002/med.20243en_US
dc.identifier.urihttp://hdl.handle.net/1808/24568
dc.descriptionThis is the peer reviewed version of the following article: Manikwar, P., Kiptoo, P., Badawi, A. H., Büyüktimkin, B. and Siahaan, T. J. (2012), Antigen-specific blocking of CD4-Specific immunological synapse formation using BPI and current therapies for autoimmune diseases. Med Res Rev, 32: 727–764. doi:10.1002/med.20243, which has been published in final form at http://doi.org/10.1002/med.20243. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
dc.description.abstractIn this review, we discuss T-cell activation, etiology, and the current therapies of autoimmune diseases (i.e., MS, T1D, and RA). T-cells are activated upon interaction with antigen-presenting cells (APC) followed by a “bull’s eye”-like formation of the immunological synapse (IS) at the T-cell–APC interface. Although the various disease-modifying therapies developed so far have been shown to modulate the IS and thus help in the management of these diseases, they are also known to present some undesirable side effects. In this study, we describe a novel and selective way to suppress autoimmunity by using a bifunctional peptide inhibitor (BPI). BPI uses an intercellular adhesion molecule-1 (ICAM-1)-binding peptide to target antigenic peptides (e.g., proteolipid peptide, glutamic acid decarboxylase, and type II collagen) to the APC and therefore modulate the immune response. The central hypothesis is that BPI blocks the IS formation by simultaneously binding to major histocompatibility complex-II and ICAM-1 on the APC and selectively alters the activation of T cells from TH1 to Treg and/or TH2 phenotypes, leading to tolerance.en_US
dc.publisherWileyen_US
dc.subjectAutoimmune diseasesen_US
dc.subjectimmunological synapseen_US
dc.subjectBifunctional peptide inhibitor (BPI)en_US
dc.subjectAntigenic peptideen_US
dc.titleAntigen-Specific Blocking of CD4-Specific Immunological Synapse Formation Using BPI and Current Therapies for Autoimmune Diseasesen_US
dc.typeArticleen_US
kusw.kuauthorManikwar, Prakash
kusw.kuauthorKiptoo, Paul
kusw.kuauthorBadawi, Ahmed H.
kusw.kuauthorBüyüktimkin, Barlas
kusw.kuauthorSiahaan, Teruna J.
kusw.kudepartmentPharmaceutical Chemistryen_US
kusw.oanotesPer SHERPA/RoMEO 6/22/2017: Author's Pre-print: green tick author can archive pre-print (ie pre-refereeing) Author's Post-print: grey tick subject to Restrictions below, author can archive post-print (ie final draft post-refereeing) Restrictions:

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dc.identifier.doi10.1002/med.20243en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC4441537en_US
dc.rights.accessrightsopenAccess


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