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Sun AC, Ou D, Luciani DS, et al. B7-H4 as a protective shield for pancreatic islet beta cells. World J Diabetes. 2014;5(6):739-46doi: 10.4239/wjd.v5.i6.739.
Sun, A. C., Ou, D., Luciani, D. S., & Warnock, G. L. (2014). B7-H4 as a protective shield for pancreatic islet beta cells. World journal of diabetes, 5(6), 739-46. https://doi.org/10.4239/wjd.v5.i6.739
Sun, Annika C, et al. "B7-H4 as a protective shield for pancreatic islet beta cells." World journal of diabetes vol. 5,6 (2014): 739-46. doi: https://doi.org/10.4239/wjd.v5.i6.739
Sun AC, Ou D, Luciani DS, Warnock GL. B7-H4 as a protective shield for pancreatic islet beta cells. World J Diabetes. 2014 Dec 15;5(6):739-46. doi: 10.4239/wjd.v5.i6.739. PMID: 25512776; PMCID: PMC4265860.
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World J Diabetes. 2014 Dec 15;5(6):739-46. doi: 10.4239/wjd.v5.i6.739.

B7-H4 as a protective shield for pancreatic islet beta cells.

World journal of diabetes

Annika C Sun, Dawei Ou, Dan S Luciani, Garth L Warnock

Affiliations

  1. Annika C Sun, Dawei Ou, Dan S Luciani, Garth L Warnock, Department of Surgery, University of British Columbia, Vancouver BC V5Z 4E3, Canada.

PMID: 25512776 PMCID: PMC4265860 DOI: 10.4239/wjd.v5.i6.739

Abstract

Auto- and alloreactive T cells are major culprits that damage β-cells in type 1 diabetes (T1D) and islet transplantation. Current immunosuppressive drugs can alleviate immune-mediated attacks on islets. T cell co-stimulation blockade has shown great promise in autoimmunity and transplantation as it solely targets activated T cells, and therefore avoids toxicity of current immunosuppressive drugs. An attractive approach is offered by the newly-identified negative T cell co-signaling molecule B7-H4 which is expressed in normal human islets, and its expression co-localizes with insulin. A concomitant decrease in B7-H4/insulin co-localization is observed in human type 1 diabetic islets. B7-H4 may play protective roles in the pancreatic islets, preserving their function and survival. In this review we outline the protective effect of B7-H4 in the contexts of T1D, islet cell transplantation, and potentially type 2 diabetes. Current evidence offers encouraging data regarding the role of B7-H4 in reversal of autoimmune diabetes and donor-specific islet allograft tolerance. Additionally, unique expression of B7-H4 may serve as a potential biomarker for the development of T1D. Future studies should continue to focus on the islet-specific effects of B7-H4 with emphasis on mechanistic pathways in order to promote B7-H4 as a potential therapy and cure for T1D.

Keywords: Autoimmunity; Biomarker; Co-stimulation blockade; Diabetes mellitus; Transplantation

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