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 .
Elimination of T cell reactivity to pancreatic β cells and partial preservation of β cell activity by peptide blockade of LFA-1:ICAM-1 interaction in the NOD mouse model
dc.contributor.author | Dotson, Abby L. | |
dc.contributor.author | Novikova, Lesya | |
dc.contributor.author | Stehno-Bittel, Lisa | |
dc.contributor.author | Benedict, Stephen H. | |
dc.date.accessioned | 2017-06-07T18:54:52Z | |
dc.date.available | 2017-06-07T18:54:52Z | |
dc.date.issued | 2013-08 | |
dc.identifier.citation | Dotson, A. L., Novikova, L., Stehno-Bittel, L., & Benedict, S. H. (2013). Elimination of T cell reactivity to pancreatic β cells and partial preservation of β cell activity by peptide blockade of LFA-1:ICAM-1 interaction in the NOD mouse model. Clinical Immunology (Orlando, Fla.), 148(2), 149–161. http://doi.org/10.1016/j.clim.2013.04.016 | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/24409 | |
dc.description.abstract | In insulin dependent diabetes mellitus (T1D), self-reactive T cells infiltrate pancreatic islets and induce beta cell destruction and dysregulation of blood glucose. A goal is to control only the self-reactive T cells, leaving the remainder of the T cell population free to protect the host. One approach is blockade of the second signal for T cell activation while allowing the first (antigen-specific) signal to occur. This work proposes that small peptides that block interaction of second signals delivered through the counter receptors LFA-1:ICAM-1 will induce attacking T cells (receiving the antigen signal) to become anergic or undergo apoptosis. In NOD mice, the peptides eliminated T cell reactivity against pancreatic antigens and reduced cellular infiltration into islets, which retained stronger density of insulin staining at five weeks after cessation of therapy. In in vitro studies the peptides induced nonresponsiveness during activation of T cells from mice and from human peripheral blood. | en_US |
dc.publisher | Elsevier | en_US |
dc.rights | This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | en_US |
dc.subject | Peptide costimulatory blockade | en_US |
dc.subject | Diabetes | en_US |
dc.subject | Autoimmunity | en_US |
dc.subject | T cell tolerance | en_US |
dc.subject | ICAM-1:LFA-1 | en_US |
dc.subject | NOD mice | en_US |
dc.title | Elimination of T cell reactivity to pancreatic β cells and partial preservation of β cell activity by peptide blockade of LFA-1:ICAM-1 interaction in the NOD mouse model | en_US |
dc.type | Article | en_US |
kusw.kuauthor | Dotson, Abby L. | |
kusw.kuauthor | Benedict, Stephen H. | |
kusw.kudepartment | Molecular Biosciences | en_US |
dc.identifier.doi | 10.1016/j.clim.2013.04.016 | en_US |
dc.identifier.orcid | https://orcid.org/0000-0002-8879-6124 | |
kusw.oaversion | Scholarly/refereed, author accepted manuscript | en_US |
kusw.oapolicy | This item meets KU Open Access policy criteria. | en_US |
dc.identifier.pmid | PMC3770271 | en_US |
dc.rights.accessrights | openAccess |
Files in this item
This item appears in the following Collection(s)
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.