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Leukotriene B4 in dendritic cells: impact in the immune response in type 1 Diabetes

Grant number: 14/21175-6
Support Opportunities:Scholarships in Brazil - Post-Doctoral
Effective date (Start): April 01, 2015
Effective date (End): September 30, 2018
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Acordo de Cooperação: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Sônia Jancar
Grantee:Marco Antonio Pires Camilo Lapa
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:13/15719-0 - Association of receptors for lipid mediators with PRRs in macrophages and dendritic cells, AP.TEM
Associated scholarship(s):17/08951-5 - Effect of leukotriene B4 receptors in dendritic cell function in type 1 diabetes mice model, BE.EP.PD


Diabetes mellitus is a metabolic disorder with a multifactorial origin, characterized by a failure in insulin production, in insulin function, or both. Several complications can arise from this illness, many of them derive from a state of low and sustained systemic inflammation, known as Sterile Inflammation (SI) that is characterized by the presence of elevated levels of pro-inflammatory cytokines such as TNF-±, IL-1± e IL-1² in the circulation. Recently, it was demonstrated that the in type 1 diabetes (T1D) there is high systemic production of leukotriene (LT) B4, which are responsible for the high levels of pro-inflammatory cytokines in the circulation. This lipid mediator affects macrophages by inducing an increase in the expression of MyD88, the adaptor molecule of IL1 and toll like receptors. The MyD88 molecule is primarily utilized in transduction pathways from receptors involved with inflammation and mediates the signaling that activates the NF-ºB pathway. In this project, we intend to evaluate the role of LTB4 on dendritic cells (DCs), myeloid cells that are the link between innate and adaptive immune responses. As T1D is an autoimmune disease mediated by T cells, it is of relevance to study how to modulate DCs function. DCs express the high affinity receptor for LTB4, the BLT-1, but the effect of this receptor activation on DCs function remains to be determined. We aim to study the impact of the increased systemic levels of LTB4 found in T1D mice in DCs and its consequences on the immune response in diabetics. (AU)

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