Clayton E. Mathews, PhD
Associate Professor

Dept. of Pathology, Immunology and Laboratory Medicine 
University of Florida College of Medicine 
PO Box 100275 
Gainesville, FL 32610-0275

Office Location and Express Mail address:
Dept. of Pathology, Immunology and Laboratory Medicine 
University of Florida 
College of Medicine 
JHMHSC R4-204 (Office) 
JHMHSC R4-156 (Lab 1) 
JHMHSC R4-183 (Lab 2) 
1600 SW Archer Rd 
Gainesville, FL 32610-0275

Office: 352-392-9803
Fax: 352-392-5393
Grants Assistant: Christy Popp (352) 392-2483
Email: clayton.mathews@pathology.ufl.edu

Currently Involved In:

Dr. Mathews’ studies have forged a new path in the understanding of autoimmune diabetes. While the majority of the field focuses on identifying defects in cells of the immune system, the guiding hypothesis of Dr. Mathews’ research is that insulin secreting pancreatic beta cells are active contributors to the autoimmune process in T1D. The initial publications from Dr. Mathews demonstrating that pancreatic islets had down regulated self-defenses, ands that this reduction was important in the initiation of diabetes. The extension of this work strongly supported the hypothesis that beta cells play an active role in the pathogenesis of diabetes. The findings demonstrated that islets varied in their resistance to autoimmune destruction and further that islets from different donors ranged from highly susceptible to extremely resistant to damage. These novel findings proved to be influential because, prior to this paper! , there was no evidence suggesting that beta cells could resist autoimmune destruction. Dr. Mathews’ investigations have provided the proof of concept for many subsequent therapy studies y both his and other groups. These findings also led Dr. Mathews a postulate that there are genetic factors expressed at the level of the pancreatic islet that provide resistance to autoimmune diabetes. His successive publications have supported this hypothesis and have identified a gene (mt-Nd2) that is responsible for protection as well as to the identification of the signaling pathways that can be blocked inhibiting beta cell death without modifying beta cell insulin secretory activity. The discovery of genes that pancreatic islets employ to ward off autoimmune effector mechanisms have important ramifications for transplantation, stem cell engineering, and future genetic and pharmacological diabetes preventative therapies.


Related Links:


Curriculum Vitae (click to download MS-Word document)

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