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, Tania orcid.org/0000-0001-5810-8063 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 1521-4141 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 Free to Read? Yes Persistent URL http://hdl.handle.net/10536/DRO/DU:30028167 Document type: Journal Article Collections: Faculty of Health School of Medicine Open Access Collection Related Links Link Description Link to full-text (open access)   Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. 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 drosupport@deakin.edu.au. Versions Version Filter Type Thu, 01 Apr 2010, 16:30:49 EST Thu, 08 Apr 2010, 10:12:44 EST Fri, 16 Apr 2010, 09:27:05 EST Tue, 10 Sep 2013, 15:47:56 EST Mon, 16 Jun 2014, 15:18:33 EST Fri, 02 Oct 2020, 10:35:31 EST Filtered Full Citation counts:   Cited 62 times in TR Web of Science Cited 66 times in Scopus Search Google Scholar Access Statistics: 955 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 drosupport@deakin.edu.au.