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World J Diabetes. Dec 15, 2014; 5(6): 739-746
Published online Dec 15, 2014. doi: 10.4239/wjd.v5.i6.739
Published online Dec 15, 2014. doi: 10.4239/wjd.v5.i6.739
B7-H4 as a protective shield for pancreatic islet beta cells
Annika C Sun, Dawei Ou, Dan S Luciani, Garth L Warnock, Department of Surgery, University of British Columbia, Vancouver BC V5Z 4E3, Canada
Author contributions: Sun AC wrote the paper; Luciani DS contributed to manuscript editing; Ou D and Warnock GL contributed to manuscript editing, and to studies reported/reviewed here.
Supported by CIHR, JDRF, and the UBC Hospital Foundation
Correspondence to: Garth L Warnock, MSc, MD, Department of Surgery, Vancouver General Hospital, University of British Columbia, 3109-910 West 10th Ave, Vancouver BC V5Z 4E3, Canada. garth.warnock@vch.ca
Telephone: +1-604-8754111 Fax: +1-604-8754036
Received: May 29, 2014
Revised: August 16, 2014
Accepted: September 6, 2014
Published online: December 15, 2014
Revised: August 16, 2014
Accepted: September 6, 2014
Published online: December 15, 2014
Core Tip
Core tip: Onset of type 1 diabetes is driven by defects in immune regulation, resulting in β-cell autoimmunity. However, there may be mechanisms inherent to the β-cell that may prevent or slow development of autoimmunity and progression of disease. One such factor is B7-H4, which acts at the islet-immune interface to defend β-cells from autoimmune diabetes and to protect transplanted islet allografts.