CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses

被引:64
作者
Hansen, DS [1 ]
Siomos, MA [1 ]
de Koning-Ward, T [1 ]
Buckingham, L [1 ]
Crabb, BS [1 ]
Schofield, L [1 ]
机构
[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia
关键词
malaria; antibody responses; NKT cells; splenomegaly; CD1;
D O I
10.1002/eji.200323666
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CD1d-restricted NKT cells are a novel T cell lineage with unusual features. They co-express some NK cell receptors and recognize glycolipid antigens through an invariant T cell receptor (TCR) in the context of CD1d molecules. Upon activation through the TCR, NKT cells produce large amounts of IFN-gamma and IL-4. It has been proposed that rapid cytokine output by activated NKT cells may induce bystander activation of other lymphoid lineages. The impact of CD1d-restricted NKT cell activation in the induction of B cell-mediated immune responses to infection is still unclear. We show here that CD1-restricted NKT cells contribute to malarial splenomegaly associated with expansion of the splenic B cell pool and enhance parasite-specific antibody formation in response to Plasmodium berghei infection. The increased B cell-mediated response correlates with the ability of NKT cells to promote Th2 immune responses. Additionally, antibody responses against the glycosylphosphatidylinositol (GPI)-anchored protein merozoite surface protein 1 (MSP-1) were found to be significantly lower in CD1(-/-) mice compared to wild-type animals. P. berghei-infected MHC class II (MHCII)(-/-) mice also generated antibodies against MSP-1, suggesting that antibody production against GPI-anchored antigens in response to malaria infection can arise from both MHCII-dependent and independent pathways.
引用
收藏
页码:2588 / 2598
页数:11
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