Alfa2a/c adrenergic receptors-deficient mice as an animal model to study the influence of the sympathetic nervous system on the experimental autoimmune encephalomyelitis development

• Grant number: 14/24156-2
• Support Opportunities: Regular Research Grants
• Start date: March 01, 2015
• End date: February 28, 2018
• 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. Indeed, immune cells, including dendritic cells (DCs) and CD4+T cells, express adrenergic receptors, mainly the ²2 adrenergic receptor (²2AR), being able to receive signals coming from the SNS. However, we still know very little on how SNS activity may influence the generation of adaptive immune responses and the occurrence of autoimmune diseases. Experimental autoimmune encephalomyelitis (EAE) is the animal model of multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (CNS) mediated by Th1 e Th17 cells. This project aims at studying the influence of the SNS on EAE induction and also on the immune effector response underlying its development. In order to accomplish our aims we propose the utilization of alpha2a/c adrenergic receptor-deficient mice as a model of SNS hyperactivity. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

TAKENAKA, MAISA C.; GUERESCHI, MARCIA G.; BASSO, ALEXANDRE S.. Neuroimmune interactions: dendritic cell modulation by the sympathetic nervous system. SEMINARS IN IMMUNOPATHOLOGY, v. 39, n. 2, p. 165-176, FEB 2017. (14/24156-2, 13/13110-9, 08/58564-9)

ARAUJO, LEANDRO PIRES; MARICATO, JULIANA TERZI; GUERESCHI, MARCIA GRANDO; TAKENAKA, MAISA CARLA; NASCIMENTO, VANESSA M.; DE MELO, FILIPE MENEGATTI; QUINTANA, FRANCISCO J.; BRUM, PATRICIA C.; BASSO, ALEXANDRE S.. The Sympathetic Nervous System Mitigates CNS Autoimmunity via beta 2-Adrenergic Receptor Signaling in Immune Cells. CELL REPORTS, v. 28, n. 12, p. 3120+, SEP 17 2019. (11/02738-1, 14/24156-2, 08/58564-9)