674 research outputs found

    Boosting Adaptive Immunity: A New Role for PAFR Antagonists.

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    We have previously shown that the Platelet-Activating Factor Receptor (PAFR) engagement in murine macrophages and dendritic cells (DCs) promotes a tolerogenic phenotype reversed by PAFR-antagonists treatment in vitro. Here, we investigated whether a PAFR antagonist would modulate the immune response in vivo. Mice were subcutaneously injected with OVA or OVA with PAFR-antagonist WEB2170 on days 0 and 7. On day 14, OVA-specific IgG2a and IgG1 were measured in the serum. The presence of WEB2170 during immunization significantly increased IgG2a without affecting IgG1 levels. When WEB2170 was added to OVA in complete Freund's adjuvant, enhanced IgG2a but not IgG1 production was also observed, and CD4+ FoxP3+ T cell frequency in the spleen was reduced compared to mice immunized without the antagonist. Similar results were observed in PAFR-deficient mice, along with increased Tbet mRNA expression in the spleen. Additionally, bone marrow-derived DCs loaded with OVA were transferred into naïve mice and their splenocytes were co-cultured with fresh OVA-loaded DCs. CD4(+) T cell proliferation was higher in the group transferred with DCs treated with the PAFR-antagonist. We propose that the activation of PAFR by ligands present in the site of immunization is able to fine-tune the adaptive immune response

    Two Generations of Hexagonal CaAl_2Si_2O_8 (Dmisteinbergite) in the Type B2 FUN CAI STP-1

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    Dmisteinbergite (dmist) is a metastable hexag-onal form of CaAl_2Si_2O_8, with space group of P6_3/mcm, a = 5.10Å and c = 14.72Å [1]. First occurrence of meteoritic dmist has been reported in the Allende Type B2 FUN CAI STP-1 [2], where it appears to have crystallized from a ^(16)O-rich (Δ^(17)O ~ −25‰) silicate melt via rapid cooling [3]. Here we report on an-other textural occurrence of dmist in STP-1 - ^(16)O-poor (Δ^(17)O ~ −2‰) fine-grained crystals in alteration zone of the inclusion

    Association of serum immunoglobulin G (IgG) levels against two periodontal pathogens and prothrombotic state: a clinical pilot study

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    <p>Abstract</p> <p>Objective</p> <p>Periodontitis is associated with cardiovascular diseases (CVD). In our previous studies a prothrombotic state has been observed in periodontitis, which contributes to the risk of CVD. The aim of this study was to investigate whether serum IgG levels against <it>Aggregatibacter actinomycetemcomitans (Aa) </it>and <it>Porphyromonas gingivalis (Pg) </it>in periodontitis were associated with a prothrombotic state.</p> <p>Materials and methods</p> <p>Patients with moderate (n = 38) and severe periodontitis (n = 30) and controls (n = 24) were recruited. We explored correlations between serum anti-<it>Aa </it>and anti-<it>Pg </it>IgG and plasma levels of markers of prothrombotic state (von Willebrand Factor [vWF], prothrombin fragment 1+2 [F1+2], plasminogen activator inhibitor-1 [PAI-1] and D-dimer). Multivariate analyses were performed considering several major potential contributing factors.</p> <p>Results</p> <p>Periodontitis patients showed higher anti-<it>Aa </it>IgG (<it>p </it>= 0.015) than controls but not for <it>Pg </it>(<it>p </it>= 0.320). In periodontitis patients, body mass index and anti-<it>Aa </it>IgG showed a positive correlation with vWF (β = 0.297, <it>p </it>= 0.010 and β = 0.248, <it>p </it>= 0.033 respectively).</p> <p>Conclusions</p> <p>In periodontitis, infection with <it>Aa </it>together with other well accepted risk factors for CVD, may play a role in increasing the risk for prothrombotic state.</p
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