CD36 modulates proinflammatory cytokine responses to Plasmodium falciparum glycosylphosphatidylinositols and merozoites by dendritic cells

被引:13
|
作者
Kumar, S. [1 ]
Gowda, N. M. [1 ]
Wu, X. [1 ]
Gowda, R. N. [1 ]
Gowda, D. C. [1 ]
机构
[1] Penn State Univ, Coll Med, Dept Biochem & Mol Biol, Milton S Hershey Med Ctr, Hershey, PA 17033 USA
基金
美国国家卫生研究院;
关键词
CD36; Dendritic cells; Glycosylphosphatidylinositols; Merozoites; Plasmodium falciparum; Proinflammatory cytokines; Toll-like receptors; TUMOR-NECROSIS-FACTOR; INTERCELLULAR-ADHESION MOLECULE-1; VASCULAR ENDOTHELIAL-CELLS; TOLL-LIKE RECEPTOR; INFECTED ERYTHROCYTES; FATAL MALARIA; SERUM-LEVELS; FACTOR-ALPHA; IFN-GAMMA; EXPRESSION;
D O I
10.1111/j.1365-3024.2012.01367.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Studies have shown that glycosylphosphatidylinositols (GPIs) of Plasmodium falciparum activate macrophages mainly through Toll-like receptor 2 (TLR2)-mediated signalling and to certain extent through TLR4-mediated signalling to induce proinflammatory cytokine production. However, the ability of parasite GPIs to activate dendritic cells (DCs) has not been reported. Here, we show that parasite GPIs efficiently activate DCs through TLR2-mediated signalling mechanism and induce the production of TNF-a and IL-12. We also studied the role of scavenger receptor CD36 in P. falciparum GPI- and merozoite-induced cytokine responses by DCs. The results indicate that CD36 modulates the cytokine-inducing activity of the parasite GPIs by collaborating with TLR2 in DCs. Furthermore, our data reveal that CD36 modulates the activity of P. falciparum merozoites, likely by the contribution of phagocytosis-coupled CD36-mediated signalling to the signalling induced by merozoites. Altogether, these results contribute towards understanding of signalling mechanisms in malaria parasite-induced activation of the innate immune system.
引用
收藏
页码:372 / 382
页数:11
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