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CD13 is a novel mediator of monocytic/endothelial cell adhesion
Author(s) -
MinaOsorio Paola,
Winnicka Beata,
O'Conor Catherine,
Grant Christina L.,
Vogel Lotte K.,
RodriguezPinto Daniel,
Holmes Kathryn V.,
Ortega Enrique,
Shapiro Linda H.
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1107802
Subject(s) - microbiology and biotechnology , biology , cell adhesion molecule , cell adhesion , endothelial stem cell , immunoglobulin superfamily , adhesion , cell–cell interaction , monocyte , leukocyte trafficking , inflammation , cell , immunology , chemokine , chemistry , in vitro , biochemistry , organic chemistry
During inflammation, cell surface adhesion molecules guide the adhesion and migration of circulating leukocytes across the endothelial cells lining the blood vessels to access the site of injury. The transmembrane molecule CD13 is expressed on monocytes and endothelial cells and has been shown to mediate homotypic cell adhesion, which may imply a role for CD13 in inflammatory monocyte trafficking. Here, we show that ligation and clustering of CD13 by mAb or viral ligands potently induce myeloid cell/endothelial adhesion in a signal transduction‐dependent manner involving monocytic cytoskeletal rearrangement and filopodia formation. Treatment with soluble recombinant (r)CD13 blocks this CD13‐dependent adhesion, and CD13 molecules from monocytic and endothelial cells are present in the same immunocomplex, suggesting a direct participation of CD13 in the adhesive interaction. This concept is strengthened by the fact that activated monocytic cells adhere to immobilized recombinant CD13. Furthermore, treatment with anti‐CD13 antibodies in a murine model of peritonitis results in a decrease in leukocyte infiltration into the peritoneum, suggesting a potential role for CD13 in leukocyte trafficking in vivo. Therefore, this work supports a new direction for CD13 biology, where these cell surface molecules act as true molecular interfaces that induce and participate in critical inflammatory cell interactions.