The concept that the nervous and the immune systems interact is already well established. However, this approach is still rarely used when projects are outlined to better understand the events involved in the generation and regulation of adaptive immune responses. The sympathetic nervous system (SNS) is one of the ways by which the immune and the nervous systems interact. Therefore, it is known that lymphoid organs such as thymus, spleen and lymph nodes receive intense sympathetic innervation, namely nerve fibers that use as main mediators of their actions catecholamines (norepinephrine and dopamine) and neuropeptide Y (NPY). The anatomy of the sympathetic innervation in the spleen and lymph nodes suggests that processes such as antigen presentation, activation and differentiation of T cells may be influenced by the SNS. Furthermore, dendritic cells and CD4+ T cells express receptors for catecholamines and NPY, which enables them to receive signals from the activity of the SNS. The influence of the SNS in the development of adaptive immune responses seems to have biological relevance since studies have shown that chemical denervation of SNS fibers leads to changes in the course of the disease in experimental models of autoimmunity such as arthritis and lupus. However, very little is known on how the SNS modulates the course of immune responses. Thus, this project aims to study how the SNS, ie, noradrenaline and NPY, modulate the development of experimental autoimmune encephalomyelitis and adaptive immune response involved in the pathophysiology of the disease.
News published in Agência FAPESP Newsletter about the scholarship: