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Blood, 17 September 2009, Vol. 114, No. 12, pp. 2411-2416. Prepublished online as a Blood First Edition Paper on July 20, 2009; DOI 10.1182/blood-2009-04-211417. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2009-04-211417v1 114/12/2411    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Allan, L. L. Articles by van den Elzen, P. PubMed PubMed Citation Articles by Allan, L. L. Articles by van den Elzen, P. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Apolipoprotein-mediated lipid antigen presentation in B cells provides a pathway for innate help by NKT cells Lenka L. Allan1, Katrin Hoefl1, Dong-Jun Zheng1, Brian K. Chung1, Frederick K. Kozak2, Rusung Tan1,3, and Peter van den Elzen1,3 1 Department of Pathology and Laboratory Medicine, University of British Columbia, Child and Family Research Institute; and 2 Division of Pediatric Otolaryngology and 3 Department of Pathology and Laboratory Medicine, Children's and Women's Hospital of British Columbia, Vancouver, BC Natural killer T (NKT) cells are innate-like lymphocytes that recognize lipid antigens and have been shown to enhance B-cell activation and antibody production. B cells typically recruit T-cell help by presenting internalized antigens recognized by their surface antigen receptor. Here, we demonstrate a highly efficient means whereby human B cells present lipid antigens to NKT cells, capturing the antigen using apolipoprotein E (apoE) and the low-density lipoprotein receptor (LDL-R). ApoE dramatically enhances B-cell presentation of alpha-galactosylceramide (GalCer), an exogenous CD1d presented antigen, inducing activation of NKT cells and the subsequent activation of B cells. B cells express the LDL-R on activation, and the activation of NKT cells by B cells is completely LDL-R dependent, as shown by blocking experiments and the complete lack of presentation when using apoE2, an isoform of apoE incapable of LDL-R binding. The dependence on apoE and the LDL-R is much more pronounced in B cells than we had previously seen in dendritic cells, which can apparently use alternate pathways of lipid antigen uptake. Thus, B cells use an apolipoprotein-mediated pathway of lipid antigen presentation, which constitutes a form of innate help for B cells by NKT cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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