NPY in the regulation of autoimmune Th1 cells

Substantial evidence indicates a dysfunctional communication between the sympathetic nervous system and the immune system in Th1-mediated autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis. In this Opinion, we propose that the sympathetic regulation of immunity is not only mediated by catecholamines but also involves neuropeptide Y (NPY), an additional postganglionic SNS transmitter that is shown to modulate various immunological functions in vitro and in vivo. Based on recent experimental findings, we believe that a more precise understanding of the role of NPY in the regulation of autoimmune Th1 cells will provide novel insights into the neuroimmunological basis of autoimmunity.

Sammy Bedoui^a, Sachiko Miyake^c, Rainer H. Straub^b, Stephan von Hörsten^a and Takashi Yamamura^c,

^aDepartment of Functional and Applied Anatomy, Medical School of Hannover, 30625 Hannover, Germany

^bDepartment of Internal Medicine I, University Hospital Regensburg, 93042 Regensburg, Germany

^cDepartment of Immunology, National Institute of Neuroscience, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan

Available online 20 August 2004.