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Evaluation of extracellular ATP and P2X7 receptor in t CD4+ lymphocytes modulation during pulmonary inflammation

Grant number: 18/18664-6
Support type:Scholarships in Brazil - Master
Effective date (Start): January 01, 2019
Effective date (End): October 31, 2020
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Maria Regina D'Império Lima
Grantee:Bruna de Gois Macêdo
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Understanding how tissue damage affects the development of inflammatory pulmonary processes, may contribute to the development of new therapies for various human respiratory conditions. Among the cells of the immune system, CD4 + T lymphocytes play a central role in the targeting and maintenance of pulmonary pathologies. These cells contributes in several forms with pulmonary inflammation, since they have a capability of polarization into subpopulations, such as Th1, Th2, Th17, and Treg, which act in particular ways through the production of different cytokines and molecules. Little is known about the influence of damage and stress cells-signaling-molecules into the CD4 + T lymphocytes polarization. Among signs of damage, extracellular ATP seems to develop fundamental role in the establishment of inflammation. This molecule acts on receptors such as P2X7, promoting cell activation, differentiation and recruitment. Thus, the present study aims to evaluate effects of extracellular ATP and P2X7 receptor on pulmonary inflammation induced by CD4 + T lymphocytes responses to a protein antigen (ovalbumin), seeking the understanding of signalling damage related to the induction and maintenance of pulmonary diseases. To reach this aim, analysis of CD4 + T lymphocytes profile of activation from OT-II mice, with or without P2X7 receptor, will be performed after immunization and challenge with OVA associated with ATP. This study should assist the understanding of how tissue damage affects CD4 + T lymphocyte response in lung inflammation. (AU)