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Junctional adhesion molecule-2 (JAM-2) promotes lymphocyte transendothelial migration

Beltraminelli, Nicola
Fasel, Nicolas
Published in Blood. 2002, vol. 100, no. 7, p. 2479-2486
Abstract The molecular mechanisms underlying lymphocyte extravasation remain poorly characterized. We have recently identified junctional adhesion molecule-2 (JAM-2), and have shown that antibodies to JAM-2 stain high endothelial venules (HEVs) within lymph nodes and Peyer patches of adult mice. Here we show that mouse lymphocytes migrate in greater numbers across monolayers of endothelioma cells transfected with JAM-2. The significance of these findings to an understanding of both normal and pathologic lymphocyte extravasation prompted us to clone the human homologue of JAM-2. We herein demonstrate that an anti-JAM-2 antibody, or a soluble JAM-2 molecule, blocks the transmigration of primary human peripheral blood leukocytes across human umbilical vein endothelial cells expressing endogenous JAM-2. Furthermore, we show that JAM-2 is expressed on HEVs in human tonsil and on a subset of human leukocytes, suggesting that JAM-2 plays a central role in the regulation of transendothelial migration.
Keywords Amino Acid SequenceAnimalsAntibodies, Monoclonal/pharmacologyBase SequenceCell Adhesion Molecules/drug effects/genetics/ physiologyCell LineCell Movement/drug effects/ physiologyEndothelium, Vascular/ physiologyGene Expression Regulation/physiologyHumansImmunoglobulins/drug effects/genetics/ physiologyLymphocytes/ physiologyMembrane Proteins/drug effects/genetics/ physiologyMiceMolecular Sequence DataSequence AlignmentSequence Homology, Amino Acid
PMID: 12239159
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JOHNSON-LEGER, Caroline et al. Junctional adhesion molecule-2 (JAM-2) promotes lymphocyte transendothelial migration. In: Blood, 2002, vol. 100, n° 7, p. 2479-2486. doi: 10.1182/blood-2001-11-0098

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Deposited on : 2010-08-27

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