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
Abby L. Dotson, Lesya Novikova, Lisa Stehno-Bittel, Stephen H. Benedict
Clinical Immunology, Volume 148, Issue 2, August 2013, Pages 149-161
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Stephen H. Benedict, PhD
Steve Benedict, PhD, is Professor of Microbiology in the Department of Molecular Biosciences at the University of Kansas. He holds degrees in Microbiology from The University of Kentucky (BS and MS) and Vanderbilt University School of Medicine (PhD). His present research interests approach two overlapping questions involving regulation of CD4+ T cells. First, how can the immune system be controlled during autoimmune disease and organ transplant rejection. This led to the manuscript in this issue, dealing with Type 1 diabetes. Second, what are the regulatory mechanisms that guide human naïve CD4+ T cells to differentiate to specific phenotypes. Recently this work has concentrated on the influence of the cellular microenvironment and how signals contributed by counter receptors located on the surfaces of adjacent cells, can control appearance of Th1, Th2 and iTreg cells during differentiation.