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.

Attached Files
Name Description MIMEType Size Downloads

Title CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses
Author(s) Hansen, Diana S.
Siomos, Mary-Anne
de Koning-Ward, TaniaORCID iD for de Koning-Ward, Tania
Buckingham, Lynn
Crabb, Brendan S.
Schofield, Louis
Journal name European journal of immunology
Volume number 33
Issue number 9
Start page 2588
End page 2598
Total pages 11
Publisher Wiley - V C H Verlag
Place of publication Weinheim, Germany
Publication date 2003
ISSN 0014-2980
Summary 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.
Language eng
DOI 10.1002/eji.200323666
Field of Research 110803 Medical Parasitology
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2003, 2003 WILEY-VCH Verlag
Persistent URL

Document type: Journal Article
Collection: School of Medicine
Connect to link resolver
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 59 times in TR Web of Science
Scopus Citation Count Cited 64 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 635 Abstract Views, 0 File Downloads  -  Detailed Statistics
Created: Thu, 01 Apr 2010, 16:30:49 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact