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International Immunology Advance Access originally published online on March 28, 2006
International Immunology 2006 18(5):741-753; doi:10.1093/intimm/dxl011
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© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Functional comparison of mouse CIRE/mouse DC-SIGN and human DC-SIGN

Irina Caminschi1,2,, Alexandra J Corbett3, Corina Zahra1, Mireille Lahoud1, Karen M Lucas1,2,, Mariam Sofi4, David Vremec1, Thomas Gramberg5, Stefan Pöhlmann5, Joan Curtis1, Emanuela Handman1, Serani L H van Dommelen3,6,, Peter Fleming3,6,, Mariapia A Degli-Esposti3,6,, Ken Shortman1,2, and Mark D Wright4

1 Walter and Eliza Hall Institute of Medical Research and
2 Cooperative Research Centre for Vaccine Technology, Melbourne, Victoria 3050, Australia
3 Centre for Experimental Immunology, Lions Eye Institute, Western Australia
4 Mac Farlane Burnet Institute for Medical Research and Public Health, Kronheimer Building, A&RMC, Studley Road Heidelberg, Victoria 3084, Australia
5 Institute for Clinical and Molecular Virology and Nikolaus-Fiebiger Center, University of Erlangen-Nürnberg, 91054 Erlangen, Germany
6 Immunology and Virology Program, Centre for Ophthalmology and Visual Science, University of Western Australia, Western Australia

Correspondence to: I. Caminschi; E-mail: caminschi{at}wehi.edu.au

CIRE/mDC-SIGN is a C-type lectin we originally identified as a molecule differentially expressed by mouse dendritic cell (DC) populations. Immunostaining with a CIRE/mDC-SIGN-specific mAb revealed that CIRE/mDC-SIGN is indeed on the surface of some CD4+, CD4–8– DCs and plasmacytoid pre-DCs, but not on CD8+ DCs. It has been proposed that CIRE/mDC-SIGN is the functional orthologue of human DC-SIGN (hDC-SIGN), a molecule that both enhances T cell responses and facilitates antigen uptake. We assessed if CIRE/mDC-SIGN and hDC-SIGN exhibit functional similarities. CIRE/mDC-SIGN is down-regulated upon activation, but unlike hDC-SIGN, incubation with IL-4 and IL-13 did not enhance CIRE/mDC-SIGN expression, indicating differences in gene regulation. Like hDC-SIGN, CIRE/mDC-SIGN bound mannosylated residues. However, we could detect no role for CIRE/mDC-SIGN in T cell–DC interactions and the protein did not bind to pathogens known to interact with hDC-SIGN, including Leishmania mexicana, cytomegalovirus, HIV and lentiviral particles bearing the Ebolavirus glycoprotein. The binding of CIRE/mDC-SIGN to hDC-SIGN ligands was not rescued when CIRE/mDC-SIGN was engineered to express the stalk region of hDC-SIGN. We conclude that there are significant differences in the fine specificity of the C-type lectin domains of hDC-SIGN and CIRE/mDC-SIGN and that these two molecules may not be functional orthologues.

Keywords: cell-surface molecules, dendritic cells, rodents

Transmitting editor: C. Goodnow


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