作者: Hubert Tsui , Rozita Razavi , Yin Chan , Jason Yantha , H-Michael Dosch
DOI: 10.1016/J.MOLMED.2007.07.006
关键词:
摘要: Type 1 diabetes (T1D) results from autoimmune-mediated loss of insulin-producing β-cells. Recent findings suggest that the events controlling T1D development are not only immunological, but also neuronal in nature. In non-obese diabetic (NOD) mouse model T1D, a mutant sensory neuron channel, TRPV1, initiates chronic, progressive β-cell stress, inducing islet cell inflammation. This novel mechanism organ-specific damage requires permissive, autoimmune-prone host, ascribes tissue specificity to local secretory dysfunction afferent neurons. NOD mice, normalizing this function by administration neurotransmitter substance P clears inflammation, reduces insulin resistance and restores normoglycemia. Here, we discuss neuro–immuno–endocrine model, its implications involvement neurons other autoimmune disorders. These developments might provide neuronal-based therapeutic interventions, particularly diabetes.