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

Hansen, DS; Siomos, MA; de Koning-Ward, T; Buckingham, L; Crabb, BS; Schofield, L

Author(s): Hansen, DS; Siomos, MA; de Koning-Ward, T; Buckingham, L; Crabb, BS; Schofield, L;
Details: Publication Year 2003-09,Volume 33,Issue #9,Page 2588-2598
Journal Title: EUROPEAN JOURNAL OF IMMUNOLOGY
Publication Type: Journal Article
Abstract: 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.
Publisher: WILEY-V C H VERLAG GMBH
Keywords: IMMUNOGLOBULIN-E PRODUCTION; CUTTING EDGE; T-CELLS; SPLENIC LYMPHOMA; MARGINAL ZONE; B-CELLS; MICE; CD1; ACTIVATION; PROLIFERATION
Publisher's Version: https://doi.org/10.1002/eji.200323666
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2003-09-01 12:00:00