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Inflammatory response of LDL electronegative mimotope peptides in cells of human and murine immune system

Grant number: 13/22806-7
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): January 01, 2014
Effective date (End): December 31, 2014
Field of knowledge:Health Sciences - Pharmacy
Principal researcher:Dulcineia Saes Parra Abdalla
Grantee:Felipe Wakasuqui
Home Institution: Faculdade de Ciências Farmacêuticas (FCF). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:12/51316-5 - Study of the activity of biodrugs, PPARs agonists and natural products with therapeutic potential in atherosclerosis, AP.TEM


Atherosclerosis is a chronic inflammatory disease induced by modification of low density lipoproteins (LDL). LDL particles are spherical with a core of nonpolar cholesterol esters and triglycerides surrounded by phospholipids and unesterified cholesterol and a molecule of apolipoprotein B - 100. The modification of LDL occurs by various processes leading to profiles modifications since electronegative minimally modified LDL [LDL (-)] to the oxidized LDL (oxLDL). Macrophages recognize oxLDL accumulated in the intima of the vessels through scavenger receptors, internalize modified LDL, and present the processed peptides to CD4 + T cells via MHC class II. The accumulation of lipids turn macrophages into foam cells, which die by apoptosis and contribute to the lipid content of the lesion. The immune response of the injury is modulated mainly by macrophages and T lymphocytes which trigger a protective effect or pro-atherogenic. Our group has selected two peptides by phage display technique (phage display) that are recognized by the variable portions of two monoclonal antibodies against human LDL electronegative. Therefore, this project aims to evaluate the immune response induced by these peptides in macrophages and lymphocytes, both human and murine, through techniques of Real-Time PCR and flow cytometry to evaluate gene expression and detection of cytokines involved in atherosclerosis.

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