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Migration of immature mouse DC across resting endothelium is mediated by ICAM-2 but independent of beta2-integrins and murine DC-SIGN homologues

Item Type:Article
Title:Migration of immature mouse DC across resting endothelium is mediated by ICAM-2 but independent of beta2-integrins and murine DC-SIGN homologues
Creators Name:Wethmar, K., Helmus, Y., Luehn, K., Jones, C., Laskowska, A., Varga, G., Grabbe, S., Lyck, R., Engelhardt, B., Bixel, M.G., Butz, S., Loser, K., Beissert, S., Ipe, U., Vestweber, D. and Wild, M.K.
Abstract:Immature dendritic cells (DC) reside in tissues where they initiate immune responses by taking up foreign antigens. Since DC have a limited tissue half-life, the DC pool in tissues has to be replenished constantly. This implies that precursor/immature DC must be able to cross non-activated endothelium using as yet unknown mechanisms. Here we show that immature, but not mature bone marrow-derived murine DC migrate across resting endothelial monolayers in vitro. We find that endothelial intercellular adhesion molecule-2 (ICAM-2) is a major player in transendothelial migration (TEM) of immature DC, accounting for at least 41% of TEM. Surprisingly, the ICAM-2-mediated TEM was independent of beta2-integrins, the known ICAM-2 ligands, since neither blocking of beta2-integrins with antibodies nor the use of CD18-deficient DC affected the ICAM-2-specific TEM. In humans, the C-type lectin DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN) was shown to interact with ICAM-2, suggesting a similar role in mice. However, we find that none of the murine DC-SIGN homologues mDC-SIGN, murine DC-SIGN-related molecule-1 (mSIGN-R1) and mSIGN-R3 is expressed on the surface of bone marrow-derived mouse DC. Taken together, this study shows that ICAM-2 strongly supports transmigration of immature DC across resting endothelium by interacting with ligands that are distinct from beta2-integrins and DC-SIGN homologues.
Keywords:CD18, DC-SIGN, Dendritic cells, ICAM-2, Transmigration, Animals, Mice
Source:European Journal of Immunology
ISSN:0014-2980
Publisher:Wiley
Volume:36
Number:10
Page Range:2781-2794
Date:October 2006
Official Publication:https://doi.org/10.1002/eji.200526311
PubMed:View item in PubMed

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