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. 2001 Mar 19;193(6):671–678. doi: 10.1084/jem.193.6.671

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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L-SIGN binds ICAM-3 (A) and HIV-1 gp120 (B). Adhesion of ICAM-3 and gp120 to the K562–L-SIGN and K562–DC-SIGN cells was measured with the fluorescent bead adhesion assay (reference 11). The y-axis represents the percentage of cells binding ligand-coated fluorescent beads. The L-SIGN cross-reacting mAbs AZN-D2 (20 μg/ml) and AZN-D3 (20 μg/ml) inhibit the adhesion of ICAM-3 and gp120 to L-SIGN, in contrast to the DC-SIGN–specific mAb AZN-D1 (20 μg/ml). Adhesion of both ICAM-3 and gp120 to the K562 transfectants is also inhibited by either 20 μg/ml mannan or 5 mM EGTA. Adhesion of both ligands to mock transfectants was <5%. One representative experiment out of three is shown (SD < 5%).