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Abstract
Disturbances in crosstalk between the immune system and the sympathetic nervous system (SNS) can contribute to the pathogenesis of Th1-mediated autoimmunity. Recent studies indicate that neuropeptide Y (NPY) has a major role in the regulation of Th1 responses. The precise role of NPY has been an enigma, but a recent study provides a breakthrough, demonstrating that NPY has a bimodal role as a negative regulator of T cells and an activator of antigen-presenting cell function.
View details for DOI 10.1016/J.IT.2006.02.003
View details for Web of Science ID 000237145700002
View details for PubMedID 16530483