NEW YORK, Oct. 11, 2012 /PRNewswire/ -- Islet Sciences, Inc., (OTCBB: ISLT) a biotechnology company engaged in the research, development and commercialization of patented technologies in the field of transplantation therapy for patients with diabetes, today announced the publishing of results from a study regarding the production and function of IL-12 in Islets and Beta cells. The conclusion and interpretation of the study is that these data identify beta cells as a local source of IL-12 ligand and suggest a direct role of IL-12 in mediating beta cell pathology.
Diakine Therapeutics, a wholly owned subsidiary of Islet Sciences, has compounds targeting the IL-12 pathway related to Diabetes and other endocrine disorders such as Atherosclerosis. Recently, Diakine has announced receipt of European patents along with grant support for the opportunity to address disease affected by IL-12. For more information on Diakine Therapeutics: http://www.diakine.com
The hypothesis of the study is that IL-12 is an important cytokine in early inflammatory responses and is implicated in the immune- mediated pathogenesis of pancreatic islets in diabetes. However, little is known about the direct effects of IL-12 on islets and beta cells.In this study, beta cell function, gene expression and protein production were assessed in primary human donor islets and murine beta cell lines in response to stimulation with IL-12 or a pro-inflammatory cytokine cocktail.
The pro-inflammatory cytokine cocktail induced islet dysfunction and potently increased the expression and production of IL-12 ligand and IL-12 receptor in human islets. In human islets, the receptor for IL-12 co-localised to the cell surface of insulin-producing cells. Both IL-12 ligand and IL-12 receptor are expressed in the homogeneous beta cell line INS-1. IL-12 induced changes in gene expression, including a dose-dependent upregulation of IFNγ (also known as IFNG), in INS-1 cells. A neutralising antibody to IL-12 directly inhibited IFNγ gene expression in human donor islets induced by either IL-12 or pro-inflammatory cytokine stimulation. Functionally, IL-12 impaired glucose-stimulated insulin secretion (GSIS) in INS-1 cells and human donor islets. A neutralising antibody to IL-12 reversed the beta cell dysfunction (uncoupling of GSIS or induction of caspase- 3 activity) induced by pro-inflammatory cytokines.
"This new study clearly shows IL-12 is made locally in islets and plays a role to damaged islets," stated John Steel, Chairman and CEO of Islet Sciences. "Additionally, this study provides support for Diakine to develop its new patented compounds to reduce IL-12 action."
About Islet Sciences, Inc.
Islet Sciences is a development-stage biotechnology company with patented technologies focused on transplantation therapy for people with insulin-dependent diabetes. The Company's transplantation technology includes methods for the culturing, isolation, maturation, and immunoprotection (microencapsulation) of islet cells. The Company's mission includes the introduction of commercial products with applications to cell-based replacement therapy in the healthcare marketplace. For more information: www.isletsciences.com
This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements for Islet Sciences reflect current expectations, as of the date of this press release, and involve certain risks and uncertainties. Actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors. Factors that could cause future results to materially differ from the recent results or those projected in forward-looking statements include the risks described in the Islet Science's reports filed with the Securities and Exchange Commission. The companies' further development is highly dependent on future medical and research developments and market acceptance, which is outside their control.
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SOURCE Islet Sciences, Inc.