Studying NKT cell metabolism in obesity and metabolic syndrome

• Grant number: 17/12848-5
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Effective date (Start): August 01, 2017
• Effective date (End): August 31, 2021
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Pedro Manoel Mendes de Moraes Vieira
• Grantee: Cristhiane Favero de Aguiar
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 15/15626-8 - Macrophages and T lymphocytes immunometabolism in metabolic and inflammatory diseases, AP.JP

Abstract

Obesity has been considered a global epidemic that affect millions of people worldwide. The consequences of a pathological weight gain can affect several systems, such as cardiovascular, endocrine, neurological and also the immune system. The study of the metabolism of immune cells in obesity has been the subject of several studies. Currently, the metabolic pathways are considered important mediators of these interactions in numerous inflammatory diseases. Within this context, lymphocytes have been studied for their activation profile and metabolism. However, little is known about the metabolism of a distinct population of T lymphocytes, the NKT cells. NKT cells are a subtype of T cells, found in low frequency in the body (less than 1% in the peripheral blood of mice and humans) and characterized by their reactivity to glycolipids presented in the context of an MHC class I-like molecule, called CD1d. These cells can be found in the adipose tissue of mice and humans and have a regulatory profile in this tissue, being able to produce IL-10 and IL-2 and to influence the polarization of M2 macrophages. It is also known that iNKT cells are important in the context of obesity, metabolic syndrome and diabetes. However, the studies are still controversial regarding the forms of activation of these cells and their consequence to the inflammation of the adipose tissue. Our hypothesis is that NKT cells have a metabolic profile that differs from the other lymphocytes and also that the microenvironment of the adipose tissue is capable of influencing the metabolism of these cells and impact on the development of obesity. Therefore, our aim is to study the metabolism of NKT cells in adipose tissue and its importance in obesity and metabolic syndrome.

Scientific publications

(4)

(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)

CORREA-DA-SILVA, FELIPE; PEREIRA, JESSICA A. S.; DE AGUIAR, CRISTHIANE F.; DE MORAES-VIEIRA, PEDRO M. M.. Mitoimmunitywhen mitochondria dictates macrophage function. Cell Biology International, v. 42, n. 6, p. 5-pg., 2018-06-01. (15/15626-8, 17/06225-5, 17/12848-5, 17/00079-7)

DA SILVA, FELIPE CORREA; AGUIAR, CRISTHIANE; PEREIRA, JESSICA A. S.; MONTEIRO, LAUAR DE BRITO; DAVANZO, GUSTAVO GASTAO; CODO, ANA CAMPOS; DE FREITAS, LEONARDO PIMENTEL; BERTI, ALINE SIQUEIRA; FERRUCCI, DANILO LOPES; CASTELUCCI, BIANCA GAZIERI; et al. Ghrelin effects on mitochondrial fitness modulates macrophage function. Free Radical Biology and Medicine, v. 145, p. 61-66, DEC 2019. (17/23679-0, 16/18031-8, 17/12848-5, 18/22505-0, 15/15626-8, 17/00079-7, 17/06225-5)

DE AGUIAR, CRISTHIANE FAVERO; CASTOLDI, ANGELA; AMANO, MARIANE T.; IGNACIO, ALINE; TERRA, FERNANDA FERNANDES; CRUZ, MARIO; FELIZARDO, RAPHAEL J. F.; BRAGA, TARCIO TEODORO; DAVANZO, GUSTAVO GASTAO; GAMBARINI, VICTOR; et al. Fecal IgA Levels and Gut Microbiota Composition Are Regulated by Invariant Natural Killer T Cells. INFLAMMATORY BOWEL DISEASES, v. 26, n. 5, p. 697-708, MAY 2020. (12/16794-3, 12/02270-2, 17/12848-5)

CORREA-DA-SILVA, FELIPE; PEREIRA, JESSICA A. S.; DE AGUIAR, CRISTHIANE F.; DE MORAES-VIEIRA, PEDRO M. M.. Mitoimmunitywhen mitochondria dictates macrophage function. Cell Biology International, v. 42, n. 6, SI, p. 651-655, JUN 2018. (15/15626-8, 17/12848-5, 17/06225-5, 17/00079-7)