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Published online before print August 29, 2006

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(Journal of Leukocyte Biology. 2006;80:1242-1250.)
© 2006 by Society for Leukocyte Biology

A dominant role for FcRII in antibody-enhanced dengue virus infection of human mast cells and associated CCL5 release

Michael G. Brown^*, Christine A. King^*,1,, Christine Sherren^*, Jean S. Marshall^*, and Robert Anderson^*,2

Departments of
^* Microbiology and Immunology and
Pathology, Dalhousie University, Halifax, Nova Scotia, Canada

² Correspondence: Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. E-mail: robert.anderson{at}dal.ca

ABSTRACT

Dengue virus is a major mosquito-borne human pathogen with four known serotypes. The presence of antidengue virus antibodies in the serum of individuals prior to dengue virus infection is believed to be an important risk factor for severe dengue virus disease as a result of the phenomenon of antibody-dependent enhancement operating on Fc receptor (FcR)-bearing cells. In addition to blood monocytes, mast cells are susceptible to antibody-enhanced dengue virus infection, producing a number of inflammatory mediators including IL-1, IL-6, and CCL5. Using the human mast cell-like lines KU812 and HMC-1 as well as primary cultures of human cord blood-derived mast cells (CBMC), we aimed to identify the participating FcRs in antibody-enhanced mast cell dengue virus infection, as FcRs represent a potential site for therapeutic intervention. CBMC expressed significant levels of FcRI, FcRII, and FcRIII, and mast cell-like HMC-1 and KU812 cells expressed predominantly FcRII. All four serotypes of dengue virus showed antibody-enhanced binding to KU812 cells. Specific FcRII blockade with mAb IV.3 was found to significantly abrogate dengue virus binding to KU812 cells and CBMC in the presence of dengue-specific antibody. Dengue virus infection and the production of CCL5 by KU812 cells were also inhibited by FcRII blockade.

Key Words: dengue hemorrhagic fever • FcR binding • dengue pathogenesis • virus-antibody complexes

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