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Association of receptors for lipid mediators with PRRs in macrophages and dendritic cells

Grant number: 13/15719-0
Support type:Research Projects - Thematic Grants
Duration: February 01, 2014 - January 31, 2019
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:Sônia Jancar
Grantee:Sônia Jancar
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Assoc. researchers:Ana Paula Lepique ; Carlos Henrique Cardoso Serezani ; Francisco José Oliveira Rios ; Jeffrey Bryant Travers ; Roger Chammas
Associated grant(s):15/50441-9 - Mechanisms mediating anti inflammatory effects of omega 3 fatty acids in metabolic disorders: role of lipid mediators and micro RNAs, AP.R
Associated scholarship(s):14/21175-6 - Leukotriene B4 in dendritic cells: impact in the immune response in type 1 Diabetes, BP.PD
14/17852-2 - The PAF receptor-mediated signaling as limiting factor of antitumor chemotherapy: assessment of immune response and the tumor microenvironment, BP.PD
14/17407-9 - Molecular programs involved in balance of SOCS-1/MyD88 expression in macrophages from individuals with diabetes and consequences in response to infection, BP.PD

Abstract

Macrophages and dendritic cells (DCs) present membrane receptors (PRRs) that recognize microbial structures, Toll-like receptor family being the prototypic receptors of this group. Another group of PRRs recognize altered self components such as oxidized lipids and dying cells and among them the CD36 was the most studied. Stimulation of these receptors induces early generation of lipid mediators (prostanoids, leukotrienes and PAF), cytokine and other genes transcription leading to a given cellular response. Our working hypothesis is that autocrine activation of receptors for lipid mediators in association with the engagement of PRRs, modifies macrophages and DCs phenotype, with important consequences in infection, tumor growth and clearance of dying cells. In the present study we will investigate the effect of: a) PAFR/CD36 association in tumor microenvironmental cells; b) PAFR in tumor-associated immunosuppression and tumor response to chemotherapy and irradiation; c) PAFR/TLR4 association in DCs function and immune responses in vivo; PAFR association with several TLRs on macrophages phenotype and functions; c) LTB4/TLR4 association in macrophages and its effect on the inflammation and resistance to infection in diabetes. (AU)

Articles published in Agência FAPESP about the research grant
Brazilian researchers propose new strategy to treat cancer 
New strategy can help to prevent and treat sepsis in diabetics 

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)
GUIMARAES, JOAO PEDRO TORRES; FILGUEIRAS, LUCIANO RIBEIRO; MARTINS, JOILSON OLIVEIRA; JANCAR, SONIA. Leukotriene Involvement in the Insulin Receptor Pathway and Macrophage Profiles in Muscles from Type 1 Diabetic Mice. Mediators of Inflammation, 2019. Web of Science Citations: 0.
DA SILVA JUNIOR, ILDEFONSO ALVES; DE SOUSA ANDRADE, LUCIANA NOGUEIRA; JANCAR, SONIA; CHAMMAS, ROGER. Platelet activating factor receptor antagonists improve the efficacy of experimental chemo- and radiotherapy. Clinics, v. 73, n. 1 2018. Web of Science Citations: 1.
ILDEFONSO ALVES DA SILVA JUNIOR; LUCIANA NOGUEIRA DE SOUSA ANDRADE; SONIA JANCAR; ROGER CHAMMAS. Platelet activating factor receptor antagonists improve the efficacy of experimental chemo- and radiotherapy. Clinics, v. 73, p. -, 2018.
FILGUEIRAS, LUCIANO RIBEIRO; KOGA, MARIANNA MAINARDI; QUARESMA, PAULA G.; ISHIZUKA, EDSON KIYOTAKA; MONTES, MARLISE B. A.; PRADA, PATRICIA O.; SAAD, MARIO J.; JANCAR, SONIA; RIOS, FRANCISCO J. PAFR in adipose tissue macrophages is associated with anti-inflammatory phenotype and metabolic homoeostasis. Clinical Science, v. 130, n. 8, p. 601-612, APR 1 2016. Web of Science Citations: 6.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.