RH Williams Laboratory for Diabetes Research


	Research in the Robert H. Williams Laboratory is focused on the way diabetes develops. The research is largely funded by the National Institutes of Health. The aims of the laboratory are to discover diabetes genes and to determine how these genes, together with environmental factors, allow the immune system to attack the insulin-producing cells in the islets of Langerhans in the pancreas. The immune attack is against self-antigens and these autoantigens are cloned and used in sensitive and specific assays to find individuals who are on their way to develop insulin-dependent diabetes mellitus (IDDM). Of particular importance are autoantibodies against glutamic acid decarboxylase (GAD), insulin and the IA-2 antibody which, together with genotyping for human leucocyte antigens (HLA) on chromosome 6, can be used to predict diabetes. The goal of the research is to develop methods of inducing tolerance against the autoantigens in an attempt to halt the autoimmune reaction against the insulin-producing cells. Since HLA proteins control the human immune response, it is of particular interest to find out why certain HLA types are necessary but not sufficient for the development of insulin-dependent diabetes. Spontaneously diabetic BB rats are bred to identify their diabetes genes and to develop autoantigen-specific immune suppression to prevent diabetes.

	Please peruse the links below for further information (links will open in a new window).

	Program Project Grants/ Information
	National Institutes of Health (NIH) Grant, BB Rat Program Project 2004 Additional Grants and Support Additional Grants Addendum

	Presentations of Research/ Topics
	Phenotyping Data Robert H. Williams Diabetes Research Counsel News Bulletins HLA-DQ Proteins - by Peter Hjelmstrom

	Protocols
	Gey's Phenotyping Protocol

	Research Reagent Material Transfer
	Original GAD65 Clone
	Our laboratory cloned the human islet GAD65 cDNA (Karlsen et al. Cloning and primary structure of human islet isoform of glutamic acid decarboxylase from chromosome 10. PNAS 88:8337-8341, 1991.) The GAD65 cDNA was originally available at no cost to researchers as a modified pcDNAII vector called pEx9 (Grubin et al. A novel radioligand binding assay to determine diagnostic accuracy of isoform-specific glutamic acid decarboxylase antibodies in childhoood IDDM. Diabetologia 37:344-350, 1994.). For more information, Click Here.
	Current GAD65 Clone
	In place of pEX9 we now offer the pThGAD65 human GAD65 clone at no cost that is a high efficiency in vitro expression plasmid utilizing the Promega pTnTTM vector. For more information, Click Here.