Agent-based models of malaria transmission: a systematic review.

Background: Much of the extensive research regarding transmission of malaria is underpinned by mathematical modelling. Compartmental models, which focus on interactions and transitions between population strata, have been a mainstay of such modelling for more than a century. However, modellers are increasingly adopting agent-based approaches, which model hosts, vectors and/or their interactions on an individual level.

Heme oxygenase-1 affords protection against noncerebral forms of severe malaria.

Infection by Plasmodium, the causative agent of malaria, is associated with hemolysis and therefore with release of hemoglobin from RBC. Under inflammatory conditions, cell-free hemoglobin can be oxidized, releasing its heme prosthetic groups and producing deleterious free heme. Here we demonstrate that survival of a Plasmodium-infected host relies strictly on its ability to prevent the cytotoxic effects of free heme via the expression of the heme-catabolyzing enzyme heme oxygenase-1 (HO-1; encoded by the Hmox1 gene).

Characterization of donor dendritic cells and enhancement of dendritic cell efflux with CC-chemokine ligand 21: a novel strategy to prolong islet allograft survival.

Dendritic cells (DCs) are the most potent antigen-presenting cells, yet little data are available on the differential characteristics of donor and recipient DCs (dDCs and rDCs, respectively) during the process of islet allograft rejection. DTR-GFP-DC mice provide a novel tool to monitor DC trafficking and characteristics during allograft rejection. We show rapid migration of dDCs to recipient lymphoid tissues as early as 3 h post-islet allotransplantation.

Heme oxygenase-1 is essential for and promotes tolerance to transplanted organs.

This investigation focused on obtaining a further understanding of the role of heme oxygenase-1 (HO-1) in tolerance induction. Hearts from C57BL/6 (H-2b) mice survived long-term when transplanted into BALB/c (H-2d) recipients treated with the tolerance-inducing regimen of anti-CD40L antibody (MR-1) plus donor-specific transfusion (DST). Grafts did not, however, survive long-term in (HO-1-/-) recipients given the same treatment.

Decay-accelerating factor prevents acute humoral rejection induced by low levels of anti-alphaGal natural antibodies.

Background: Hyperacute and delayed vascular rejection due to natural antibodies (NAb) present major obstacles in pig-to-primate xenotransplantation. Although "supraphysiologic" expression of human complement regulatory proteins (CRPs) can prevent hyperacute rejection in discordant xenogenic recipients, their physiologic role in the homologous setting is undefined. We have evaluated the effect of the absence of decay-accelerating factor (DAF) on cardiac allograft rejection in the presence of different levels of antidonor antibodies (Ab).

Induction of xenograft accommodation by modulation of elicited antibody responses1 2.

Background: We have established that the timing of splenectomy influences the magnitude of the xenoreactive antibody (XAb) response and thus hamster heart survival in cyclosporine (CyA)-treated rats. This model has been used to test our hypothesis that modulation of XAb responses without perturbation of complement may influence the development of graft accommodation.

Methods: Pretransplantation splenectomy (day -1/day 0) fully abrogated anti-graft IgM response, whereas a delayed procedure (day 1/day 2) caused significantly delayed (3-4 days) and decreased levels (two- to threefold) of XAb.