| Malaria is one of the most severe infectious diseases in the world and responsible for 2 millions of deaths every year. The pathogenesis of malaria is complicated, multifactor and poorly understood. And up to now, mechanisms for malaria parasite escaping from host immune attack have not been understood clearly. No malaria-derived molecule has been found in regulating the host immune response directly.Macrophage migration inhibitory factor (MIF) was a pluripotent cytokine, and ubiquitously expressed in a variety of cells, such as macrophages and lymphocytes. It exhibited an array of biological functions ranging from immune responsiveness to cell growth and induced inflammation at the interface between the innate immunity and acquired immunity. Host-derived MIF has been implicated in the pathogenesis of malaria infection, especially in malarial anemia. Recently, three Plasmodium parasite-derived MIFs, P. falciparum MIF (PfMIF), P. berghei MIF (PbMIF) and P. yoelii MIF(PyMIF), were suggested to modulate host immune-cell activity. However, the precise roles of these parasite-derived MIFs during malaria infection remain unknown.In this study, the effect of another parasite homologue of MIF (PyMIF) on mouse splenic DCs was investigated and compared the effect of its murine counterpart (MmMIF). The results showed that, PyMIF could reduce the surface expression of Toll-like receptor (TLR) 4, but not induce splenic DCs maturation. PyMIF could reduce CD11c+CD8+ DCs secretion of IL-12 and increse the secretion of TGF-β1; whereas, they could not modulate CD8"CD4+CDllb+ DCs. We also investigated the effect of splenic DCs (previously incubated with PyMIF) on CD8+T cells, the results showed that such splenic DCs could reduce CD8+T cells surface expression of CD69 and modulate the secretion of IL-2 through CD11c+CD8+ DCs but not the CTL response.These results suggest that PyMIF have some minor regulatory role of spleen DCs, CD11c+CD8+ DCs may be one of PyMIF target cells. |
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