Cellular, molecular and immunological mechanisms generated through NLRP activation

• Grant number: 14/06992-8
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: July 01, 2014
• End date: June 30, 2017
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Niels Olsen Saraiva Câmara
• Grantee: Tárcio Teodoro Braga
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches, AP.TEM
• Associated scholarship(s): 15/21168-2 - CELLULAR AND MOLECULAR MECHANISMS BEHIND NLRP3 INFLAMMASOME ACTIVATION, BE.EP.PD

Abstract

NLR (Nucleotide-binding domain, leucine-rich repeat containing protein) is a group of intracellular proteins that regulate inflammation. Despite the extensive number of studies on the activators of NLR, we still do not know how how this group of proteins is able to answer many different ligands, or what are the mechanisms of their transcriptional regulation. Induction of the inflammasome NLRP3, the most widely studied NLR, by endogenous ligands indicates that there is a potential link between the innate immune system and the maintenance of homeostasis of the organism. Although the activation of NLRP3 is a process mediated by the innate immune system, such deficiency causes a milder injury in the development of autoimmune diseases, typical diseases of an adaptive immune response profile, as in the case of EAE (Experimental Autoimmune Encephalopathy). We know, for example, besides low score disease, NLRP3 deficiency causes less lymphocytic infiltration and lower levels of IL17 and IFN³ in these animals compared with wild-type mice with EAE. It is known that microglial activation plays a crucial role in the development of EAE and that activated microglia can secrete IL1², which ultimately attract T cells and infiltrating macrophages. However, more studies about the cellular origin and the molecular mechanisms involved in inflammasome activation and subsequent development of EAE are still needed. Therefore, this present study aims to evaluate the role of the NLRP3 during the course of experimental autoimmune encephalopathy.

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)

BRAGA, TARCIO TEODORO; CORREA-COSTA, MATHEUS; SILVA, REINALDO CORREIA; CRUZ, MARIO COSTA; HIYANE, MEIRE IOSHIE; DA SILVA, JOAO SANTANA; PEREZ, KATIA REGINA; CUCCOVIA, IOLANDA MIDEA; SARAIVA CAMARA, NIELS OLSEN. CCR2 contributes to the recruitment of monocytes and leads to kidney inflammation and fibrosis development. INFLAMMOPHARMACOLOGY, v. 26, n. 2, p. 403-411, APR 2018. (14/06992-8, 12/02270-2)

BRAGA, TARCIO TEODORO; BRANDAO, WESLEY NOGUEIRA; AZEVEDO, HATYLAS; TERRA, FERNANDA FERNANDES; MELO, AMANDA CAMPELO L.; PEREIRA, FELIPE VALENCA; ANDRADE-OLIVEIRA, VINICIUS; HIYANE, MEIRE IOSHIE; PERON, JEAN PIERRE S.; SARAIVA CAMARA, NIELS OLSEN. NLRP3 gain-of-function in CD4(+) T lymphocytes ameliorates experimental autoimmune encephalomyelitis. Clinical Science, v. 133, n. 17, p. 1901-1916, SEP 13 2019. (17/05264-7, 17/22504-1, 14/06992-8)

BRAGA, TARCIO TEODORO; DAVANSO, MARIANA RODRIGUES; MENDES, DAVI; DE SOUZA, TIAGO ANTONIO; DE BRITO, ANDERSON FERNANDES; CRUZ, MARIO COSTA; HIYANE, MEIRE IOSHIE; DE LIMA, DHEMERSON SOUZA; NUNES, VINICIUS; GIAROLA, JULIANA DE FATIMA; et al. Sensing soluble uric acid by Naip1-Nlrp3 platform. CELL DEATH & DISEASE, v. 12, n. 2, FEB 5 2021. (17/05264-7, 14/06992-8)

BRAGA, TARCIO TEODORO; FORNI, MARIA FERNANDA; CORREA-COSTA, MATHEUS; RAMOS, RODRIGO NALIO; BARBUTO, JOSE ALEXANDRE; BRANCO, PAOLA; CASTOLDI, ANGELA; HIYANE, MEIRE IOSHIE; DAVANSO, MARIANA RODRIGUES; LATZ, EICKE; et al. Soluble Uric Acid Activates the NLRP3 Inflammasome. SCIENTIFIC REPORTS, v. 7, JAN 13 2017. (13/07937-8, 12/02270-2, 14/06992-8)