The Interface Between the Nervous and the Immune System in the Pathogenesis of Autoimmune Diabetes - June 15, 2011 - Neuroscience Center (NSC) Building
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The purpose of this workshop is to gain knowledge on the state-of-the-art and perspectives on the role of the central and peripheral nervous system on the pathogenesis and modulation of the inflammatory process that leads to selective beta cell destruction in type 1 diabetes (T1D) and also how the inflammatory process may affect neural control of islet cells function.

Background and Justification:  T1D is thought to be caused by an immune system that has failed to maintain tolerance to self antigens expressed by the insulin-producing beta cell. For T1D, the currently known self antigens are mainly expressed in beta cells and some are also present elsewhere in the body, including neuronal antigens. There is some evidence for functional interactions between the nervous system and the immune system but the connections between islet autoimmunity and nervous system function are not known. Thus, this workshop will help shed light on the role of the central and peripheral nervous system on the pathogenesis and modulation of the inflammatory process that leads to selective beta cell destruction in T1D and also how the inflammatory process may affect neural control of islet cells function. Elucidation of these mechanisms could open new avenues for biomarkers or therapeutics.

Research Goals and Objectives:  To discuss the role of the central and peripheral nervous system on the pathogenesis and modulation of the inflammatory process that leads to selective beta cell destruction in T1D and determine the effect of inflammation on neural control of islet cells function. The main questions that would be addressed are the following:

  1. Does autoimmunity target the islet efferent and afferent innervation, does it induce an islet neuropathy, and does it influence autoreactivity against β cells?
  2. Are neurotransmiters/neuropeptides important for β cell function, neogenesis, or regeneration?
  3. Do signals from the nervous system alter inflammation and insulin resistance?
  4. Does islet inflammation modulate islet innervation and neural function?
  5. What is the role of innervation in the defective counter-regulatory response that is seen in T1D?
  6. Are there other examples of neural involvement in tissue targeting in autoimmunity that could illuminate pathogenesis in T1D?  

Understanding the role of the central and peripheral nervous system in T1D pathogenesis is likely to provide crucial new insights into disease pathogenesis.

Organizing Committee:

Co-Chairs:

Alejandro Caicedo, Ph.D., University of Miami
Hans-Michael Dosch, M.D., Ph.D., University of Toronto
Gerald Taborsky, Jr., Ph.D., University of Washington

NIDDK:

Beena Akolkar, Ph.D., NIDDK, NIH
Michael Appel, Ph.D., NIDDK, NIH
Guillermo Arreaza-Rubin, M.D., NIDDK, NIH
Lisa Spain, Ph.D., NIDDK, NIH

For questions concerning program content, contact:

Guillermo Arreaza-Rubin, M.D.
Telephone:  (301) 594-4724
Email:  arreaza-rubing@niddk.nih.gov

Beena Akolkar, Ph.D.
Telephone:  (301) 594-8812
Email:  akolkarb@extra.niddk.nih.gov

For questions concerning meeting logistics, contact:

John Hare, M.S., CMP
Telephone:  (301) 670-4990
Email:  jhare@scgcorp.com

 

NIDDK NIH DHHS