CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses
Hansen, Diana S., Siomos, Mary-Anne, de Koning-Ward, Tania, Buckingham, Lynn, Crabb, Brendan S. and Schofield, Louis 2003, CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses, European journal of immunology, vol. 33, no. 9, pp. 2588-2598, doi: 10.1002/eji.200323666.
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CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses
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- 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 arisefrom both MHCII-dependent and independent pathways.
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