Crystallization conditions of two adjacent epidote + diopside-bearing granitic stocks, northeastern Brazil.

The Tamboril and Olho d'Água granitic stocks are part of the abundant calc-alkalic magmatic epidote-bearing granitic rocks in the Cachoeirinha-Salgueiro Terrane (CST) in the Transversal Zone Domain, northeastern Brazil. The equigranular Olho d'Água stock is composed of medium-grained clinopyroxene-amphibole-biotite tonalite; the porphyritic Tamboril stock is medium- to coarse-grained amphibole biotite ± clinopyroxene granodiorite. Abundances of clinopyroxene and epidote vary inversely in both stocks. Amphibole-rich clots are regarded as fragments from the source region captured by granodioritic/tonalitic magma during its ascent. Epidote composition in the Olho d'Água stock (Ps18-26) and in Tamboril stock (Ps17-20) is consistent with crystallization under oxygen fugacity between QFM and HM buffers. In the Olho d'Água stock, calculated values of pressure range from 5.1 to 6.6 kbar and in the Tamboril stock from 6.2 to 7.0 kbar. Solidification temperatures estimated from plagioclase-hornblende pairs in the Olho D´Água stock range from 637 to 679 °C and for Tamboril from 587 to 641 °C. Zr-saturation temperature estimates are 788 to 819 °C (Olho d'Água) and 807 to 829 °C (Tamboril). Altogether our data suggest that the studied stocks crystallized from two distinct magmatic pulses formed from fractional melting of a single amphibolitic source. These two magma pulses underwent subsequent crystallization, in a convective magmatic chamber, at rather high pressure.

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

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 IFNγ 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.

Cytokine modulation of human blood viscosity from vivax malaria patients.

Malaria is a major infectious disease in several countries and is caused by protozoa of the genus Plasmodium. In vivax malaria patients, inflammatory processes occur, as well as changes in cytokines and blood flow. The present study analyzed the cytokine modulation of blood viscosity from patients infected with Plasmodium vivax (P. vivax). Blood samples were collected from 42 non-infected individuals (control group) and 37 individuals infected with P. vivax. The IL-2, IL-4, IL-6, IL-10, TNFα, TGF-ß and IL-17 cytokine concentrations in the serum were assessed, and the blood rheological properties were determined. The analysis of blood viscosity for shear rates revealed that the blood viscosity of the infected patients was significantly greater than that of the non-infected individuals. The viscosity of the blood was greater in the infected individuals than in the non-infected subjects. The serum from individuals with P. vivax infections exhibited higher IFN-γ and IL-17 concentrations and lower TGF-ß levels. Incubation of the blood from infected individuals with IL-17 or IL-17 associated with IFN-γ reduced the viscosity to rates equivalent to the blood from non-infected individuals. Independently of cytokine modulation, no correlation was found between the parasitemia and blood viscosity of the infected patients. These data suggest that the alterations of blood viscosity are relevant as an auxiliary tool for the clinical diagnosis of disease. In malaria, erythrocytes are more sensitive to osmotic shock, and the reduction of viscosity by IL-17 may be related to a possible immunomodulator agent during infection.