Enteroendocrine hormones and cells of the immune system: impact on the metabolism, differentiation, and function

• Grant number: 21/10908-6
• Support Opportunities: Scholarships in Brazil - Master
• Start date: November 01, 2021
• End date: October 31, 2023
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Vinicius de Andrade Oliveira
• Grantee: Laura de Quadros Pereira
• Host Institution: Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil
• Associated research grant: 19/14755-0 - Shaping gut microbiota and immune system by the intestinal epithelial cells: from tissue homeostasis to diseases, AP.JP

Abstract

Enteroendocrine hormones are hormones released from the activation of enteroendocrine cells (CEE), cells that reside in the epithelial layer of the gastrointestinal tract. CEEs release these hormones from the presence of nutrients. Among these hormones are the incretins GIP (Gastric Inhibitory Polypeptide) and GLP-1 (Glucagon-like Polypeptide 1). These two hormones have the ability to release insulin by binding to its receptors on pancreatic beta cells. Dendritic cells (DC) are responsible for presenting antigens to CD4 and CD8 T lymphocytes and are considered the bridge between innate and adaptive immunity. CD4+ T lymphocytes when stimulated by DC can differentiate into different types and the activation control of these lymphocytes can be performed by the generation of regulatory T cells (Treg). Furthermore, studies have shown that the activation of GIP and GLP-1 can have an anti-inflammatory role. The hypothesis of this work is that immune system cells can undergo modulation of their activation and differentiation by the action of these receptors, aiming to elucidate the impact of activation of these receptors on different types of immune cells. The objective is to evaluate the impact of GIPR and GLP-1R receptors activation on immune system cell differentiation/activation. Thus, the expression of receptors and their modulation in dendritic cells will be evaluated, as well as the maturation of DC in the presence of GIPR and GLP-1R agonists and their potential to stimulate T lymphocytes, the modulation of receptor expression in lymphocytes CD4+ T after activation and differentiation of different subtypes, and glycolytic and oxidative metabolism of DC and CD4+ T cell subtypes after receptor stimulation. (AU)