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10.1371/journal.ppat.1006595 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006595 C5597262!5597262 !28859168     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28859168 &cmd=llinks): Failed to open stream: HTTP request failed! 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P2X7 receptor drives Th1 cell differentiation and controls the follicular helper T cell population to protect against Plasmodium chabaudi malaria |pdf=|usr=}}{{28859168 }} gab.com Text P2X7 receptor drives Th1 cell differentiation and controls the follicular helper T cell population to protect against Plasmodium chabaudi malaria JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28859168 #FOAvip 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-stage Plasmodium chabaudi malaria. The P2X7 receptor was activated in CD4 T cells following the rupture of infected erythrocytes and these cells became highly responsive to ATP during acute infection. Moreover, mice lacking the P2X7 receptor had increased susceptibility to infection, which correlated with impaired Th1 cell differentiation. Accordingly, IL-2 and IFN? secretion, as well as T-bet expression, critically depended on P2X7 signaling in CD4 T cells. Additionally, P2X7 receptor controlled the splenic Tfh cell population in infected mice by promoting apoptotic-like cell death. Finally, the P2X7 receptor was required to generate a balanced Th1/Tfh cell population with an improved ability to transfer parasite protection to CD4-deficient mice. This study provides a new insight into malaria immunology by showing the importance of P2X7 receptor in controlling the fine-tuning between Th1 and Tfh cell differentiation during P. chabaudi infection and thus in disease outcome. Twit Text FOAVip P2X7 receptor drives Th1 cell differentiation and controls the follicular helper T cell population to protect against Plasmodium chabaudi malaria ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28859168 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28859168 #FOAvip English Wikipedia <ref>{{Cite pmid|28859168 }}</ref> P2X7 receptor drives Th1 cell differentiation and controls the follicular helper T cell population to protect against Plasmodium chabaudi malaria #MMPMID28859168 Salles ÉM ; Menezes MN ; Siqueira R ; Borges da Silva H ; Amaral EP ; Castillo-Méndez SI ; Cunha I ; Cassado ADA ; Vieira FS ; Olivieri DN ; Tadokoro CE ; Alvarez JM ; Coutinho-Silva R ; D'Império-Lima MR PLoS Pathog 2017[Aug]; 13 (8 ): e1006595 PMID28859168 show ga 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-stage Plasmodium chabaudi malaria. The P2X7 receptor was activated in CD4 T cells following the rupture of infected erythrocytes and these cells became highly responsive to ATP during acute infection. Moreover, mice lacking the P2X7 receptor had increased susceptibility to infection, which correlated with impaired Th1 cell differentiation. Accordingly, IL-2 and IFN? secretion, as well as T-bet expression, critically depended on P2X7 signaling in CD4 T cells. Additionally, P2X7 receptor controlled the splenic Tfh cell population in infected mice by promoting apoptotic-like cell death. Finally, the P2X7 receptor was required to generate a balanced Th1/Tfh cell population with an improved ability to transfer parasite protection to CD4-deficient mice. This study provides a new insight into malaria immunology by showing the importance of P2X7 receptor in controlling the fine-tuning between Th1 and Tfh cell differentiation during P. chabaudi infection and thus in disease outcome. |Adoptive Transfer [MESH] |Animals [MESH] |Cell Differentiation/*immunology [MESH] |Disease Models, Animal [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Enzyme-Linked Immunospot Assay [MESH] |Erythrocytes/parasitology [MESH] |Female [MESH] |Fluorescent Antibody Technique [MESH] |In Situ Nick-End Labeling [MESH] |Lymphocyte Activation/*immunology [MESH] |Malaria/*immunology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Plasmodium chabaudi/immunology [MESH] |Receptors, Purinergic P2X7/*immunology [MESH] |T-Lymphocytes, Helper-Inducer/*immunology [MESH]P2X7 receptor drives Th1 cell differentiation and controls the follicu(epmc).pdf DeepDyve Pubget Overpricing