Journal article

P2X7 receptor drives Th1 cell differentiation and controls the follicular helper T cell population to protect against Plasmodium chabaudi malaria

Erika Machado de Salles, Maria Nogueira de Menezes, Renan Siqueira, Henrique Borges da Silva, Eduardo Pinheiro Amaral, Sheyla Ines Castillo-Mendez, Isabela Cunha, Alexandra dos Anjos Cassado, Flavia Sarmento Vieira, David Nicholas Olivieri, Carlos Eduardo Tadokoro, Jose Maria Alvarez, Robson Coutinho-Silva, Maria Regina D'Imperio-Lima

PLoS Pathogens | PUBLIC LIBRARY SCIENCE | Published : 2017

Abstract

A complete understanding of the mechanisms underlying the acquisition of protective immunity is crucial to improve vaccine strategies to eradicate malaria. However, it is still unclear whether recognition of damage signals influences the immune response to Plasmodium infection. Adenosine triphosphate (ATP) accumulates in infected erythrocytes and is released into the extracellular milieu through ion channels in the erythrocyte membrane or upon erythrocyte rupture. The P2X7 receptor senses extracellular ATP and induces CD4 T cell activation and death. Here we show that P2X7 receptor promotes T helper 1 (Th1) cell differentiation to the detriment of follicular T helper (Tfh) cells during blood..

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Grants

Awarded by Sao Paulo Research Foundation (FAPESP, Brazil)


Awarded by National Council for Scientific and Technological Development (CNPq, Brazil)


Awarded by FAPESP


Funding Acknowledgements

This work was supported by Sao Paulo Research Foundation (FAPESP, Brazil) grants, 2010/51150-4, 2013/07140-2 and 2015/20432-8 (MRDL) and National Council for Scientific and Technological Development (CNPq, Brazil) grants, 303676/2014-0 and 448765/2014-4 (MRDL). EMS received a PhD fellowship from FAPESP (2011/11053-2). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.