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The Journal of Immunology, 2002, 168: 6455-6462.
Copyright © 2002 by The American Association of Immunologists

Absence of Platelet Endothelial Cell Adhesion Molecule-1 (CD31) Leads to Increased Severity of Local and Systemic IgE-Mediated Anaphylaxis and Modulation of Mast Cell Activation1

Mae-Xhum Wong, Donna Roberts, Paul A. Bartley and Denise E. Jackson2

Division of Hematology, Hanson Institute, Institute of Medical and Veterinary Science, Adelaide, South Australia, Australia

Platelet endothelial cell adhesion molecule-1 (PECAM-1) is a newly assigned member of the Ig-immunoreceptor tyrosine-based inhibitory motif superfamily, and its functional role is suggested to be an inhibitory receptor that modulates immunoreceptor tyrosine-based activation motif-dependent signaling cascades. In this study, we hypothesized that PECAM-1 plays an essential in vivo role as a counterregulator of immediate hypersensitivity reactions. We found that PECAM-1 was highly expressed on the surface of immature bone marrow mast cells and at a lower density on mature peritoneal mast cells. Examination of skin biopsies from PECAM-1+/+ and PECAM-1-/- mice revealed that absence of PECAM-1 did not affect mast cell development or the capacity of mast cells to populate tissues. To examine whether the absence of PECAM-1 would influence immediate hypersensitivity reactions, PECAM-1+/+ and PECAM-1-/- mice were presensitized with anti-DNP mouse IgE and then challenged 20 h later with DNP-BSA or PBS. PECAM-1-/- mice exhibited elevated serum histamine concentrations after Ag stimulation compared with PECAM-1+/+ mice, indicating an increased severity of systemic IgE-mediated anaphylaxis. PECAM-1-/- mice have increased sensitivity to local cutaneous IgE-dependent anaphylaxis compared with PECAM-1+/+ mice, as assessed by greater tissue swelling of their ears and mast cell degranulation in situ. PECAM-1-/- bone marrow mast cells showed enhanced dense granule serotonin release after Fc{epsilon}RI cross-linking in vitro. These results suggest that PECAM-1 acts as a counterregulator in allergic disease susceptibility and severity and negatively modulates mast cell activation.




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