Modulation of macrophage activation profile by beta2-adrenergic signaling and its impact on EAE development

• Grant number: 20/09488-0
• Support Opportunities: Regular Research Grants
• Start date: November 01, 2020
• End date: October 31, 2022
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Alexandre Salgado Basso
• Grantee: Alexandre Salgado Basso
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

The nervous system can interact with the immune system via the sympathetic nervous system (SNS). It has been already described that lymphoid organs are richly innervated by sympathetic fibers, which exert their actions by releasing mainly catecholamines. The anatomy of the sympathetic innervation in lymphoid organs such as the spleen and lymph nodes suggests that many immune processes, including antigen presentation and, T cell activation and differentiation, may be under direct influence of the mediators released by sympathetic fibers. Recently, we have shown that SNS activity, by signaling via beta2-adrenergic receptors, inhibits the generation of encephalitogenic CD4 T cell responses mitigating experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. This project aims at studying the influence of beta2-adrenergic receptor signaling on macrophage activation profile and how this may impact the effector phase of EAE. (AU)