Journal
BLOOD
Volume 110, Issue 7, Pages 2545-2555Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2007-03-078733
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Funding
- NHLBI NIH HHS [P01 HL036028, R01 HL053993, HL36028, HL53993] Funding Source: Medline
- Medical Research Council [G9818340B] Funding Source: researchfish
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Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti-JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C-mediated monocyte retention.
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