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CUNHA, I. Participation of the P2X7 receptor in the control of splenic Tfh and B cell populations and protection against Plasmodium yoelii. 2018. 69 f. Dissertation (Master in Immunology) Institute of Biomedical Sciences, University of São Paulo, São Paulo, 2018. Immunity to malaria is short-lived and cured individuals are susceptible to reinfections. Some evidence suggests that deficiency in the production of parasitespecific antibodies may explain the difficulty in developing an effective immune response against malaria. B cells are selected in a highly regulated environment, named the germinal center, located in the secondary lymphoid organs. The interaction between follicular T cells (Tfh) and germinal center B cells allows the production of long-lived plasma cells that secrete antibodies with high affinity for the antigen and generation of memory B cells. Recent studies have shown that P2X7 receptor signaling by extracellular ATP affects the T cell response. In Plasmodium chabaudi infection, the P2X7 receptor contributes to parasite control by favoring the production of Th1 cells secreting IFN-γ to the detriment of the Tfh cell population. In this work, we aimed to evaluate the participation of the P2X7 receptor in the production of Tfh cells and germinal center B cells in mice infected with Plasmodium yoelii 17XNL. This study is justified since the protection against P. yoelli 17XNL depends mainly on antibodies, whereas IFN-γ is essential for the control of acute P. chabaudi infection. Our results show that P2X7 knockout mice (P2X7) displayed lower parasitemias than the C57BL/6 mice in the acute phase of infection. However, the time elapsed until the peak of parasitemia and control of the parasite were similar in both groups. We also observed less marked anemia in the absence of the P2X7 receptor, but this finding must be confirmed because a single experiment was performed. Infected P2X7 mice showed a greater increase in the number of CD4 T cells, Tfh cells, B cells, germinal center B cells and plasma cells in the spleen, compared to infected C57BL/6 mice. In addition, the frequencies of dead cells in the populations of CD4 T cells and B cells were lower in the absence of the P2X7 receptor. Nevertheless, in the acute phase of infection, serum levels of parasitespecific IgM and IgG2c antibodies were similar in P2X7 and C57BL/6 mice. In conclusion, this study shows that the P2X7 receptor impairs the expansion of the Tfh cell and germ center B cell populations, as well as the control of P. yoelli 17XNL malaria.

Participação do receptor P2X7 no controle das populações de células TFH e B esplênicas e na proteção contra o &gt;i&lt;Plasmodium yoelii&gt;/i&lt; 17XNL