Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites

Interleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia during Plasmodium infection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology during Plasmodium infection. Here, we summarize the role of IL-10 during murine malaria infection, focusing especially on coinfection with lethal and nonlethal strains of malaria parasites. Recent studies have demonstrated that the major sources of IL-10 are subpopulations of CD4+ T cells in humans and mice infected with Plasmodium. We also discuss the influence of innate immunity on the induction of CD4+ T cells during murine malaria coinfection

The protective effect of CD40 ligand–CD40 signalling is limited during the early phase of Plasmodium infection

Abstractγδ T cells are essential for eliminating Plasmodium berghei XAT. Because administration of the agonistic anti-CD40 antibody can induce elimination of P. berghei XAT parasites in γδ T cell-deficient mice, we considered that γδ T cells might activate dendritic cells via CD40 signalling during infection. Here we report that administration of the anti-CD40 antibody to γδ T cell-deficient mice 3–10days post-P. berghei XAT infection could eliminate the parasites. Our data suggest that dendritic cell activation via γδ T cells expressing CD40 ligand is critical during the early phase of infection

The innate immune system in host mice targets cells with allogenic mitochondrial DNA

Tumors or embryonic stem cells bearing foreign mitochondrial DNA are rejected by the innate immune system via a mechanism that depends on MyD88

Additional file 1 of Characterization of a nuclear transport factor 2-like domain-containing protein in Plasmodium berghei

Additional file 1: Figure S1. Schematic representation of the gene-targeting vector used to disrupt PBANKA_1019700, PBANKA_1101300 (SBP1) and PBANKA_0519900. Figure S2. Generation of parasites to investigate the localization of PBANKA_1019700.Figure S3. Generation of parasites to investigate the localization of PBANKA_0519900::GFP and PBANKA_1359300::GFP

IFNGR1 signaling is associated with adverse pregnancy outcomes during infection with malaria parasites

<div><p>Complicated/severe cases of placental pathology due to <i>Plasmodium falciparum</i> and <i>P</i>. <i>vivax</i>, especially adverse pregnancy outcomes during <i>P</i>. <i>vivax</i> infection, have been increasing in recent years. However, the pathogenesis of placental pathology during severe malaria is poorly understood, while responses against IFN-γ are thought to be associated with adverse pregnancy outcomes. In the present study, we explored the role of IFN-γ receptor 1 (IFNGR1) signaling in placental pathology during severe malaria using luciferase-expressing rodent malaria parasites, <i>P</i>. <i>berghei</i> NK65 (<i>Pb</i>NK65L). We detected luciferase activities in the lung, spleen, adipose tissue, and placenta in pregnant mice, suggesting that infected erythrocytes could accumulate in various organs during infection. Importantly, we found that fetal mortality in IFNGR1-deficient mice infected with <i>Pb</i>NK65L parasites was much less than in infected wild type (WT) mice. Placental pathology was also improved in IFNGR1-deficient mice. In contrast, bioluminescence imaging showed that parasite accumulation in the placentas of IFNGR1-deficient pregnant mice was comparable to that in WT mice infected with <i>Pb</i>NK65L. These findings suggest that IFNGR1 signaling plays a pivotal role in placental pathology and subsequent adverse pregnancy outcomes during severe malaria. Our findings may increase our understanding of how disease aggravation occurs during malaria during pregnancy.</p></div