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Blood, 15 April 2002, Vol. 99, No. 8, pp. 2890-2896
IMMUNOBIOLOGY
Human mast cell progenitors use  4-integrin, VCAM-1, and PSGL-1
E-selectin for adhesive interactions with human vascular endothelium
under flow conditions
Joshua A. Boyce,
Elizabeth
A. Mellor,
Brandy Perkins,
Yaw-Chyn Lim, and
Francis W. Luscinskas
From the Departments of Medicine, Pediatrics, and
Pathology, Harvard Medical School; Divisions of Rheumatology,
Immunology and Allergy, and Vascular Research, and Partners Asthma
Center, Brigham and Women's Hospital and, Boston, MA.
Mast cells (MCs) are central to asthma and other allergic diseases,
and for responses to infection and tissue injuries. MCs arise from
committed progenitors (PrMCs) that migrate from the circulation to
tissues by incompletely characterized mechanisms, and differentiate in
situ in perivascular connective tissues of multiple organs. PrMCs
derived in vitro from human cord blood were examined for adhesion
molecule expression and their ability to adhere to human umbilical vein
endothelial cells (HUVECs) under conditions that mimic physiologic
shear flow. The PrMCs expressed  4 1, low levels of 7, and the
2-integrins L2 and M2. The PrMCs also expressed PSGL-1,
but not L-selectin. At low (0.5 dynes/cm2-1.0
dynes/cm2) shear stress, PrMCs attached and rolled on
recombinant E-selectin and P-selectin and VCAM-1. An
anti-PSGL-1 monoclonal antibody (mAb) blocked
essentially all adhesion to P-selectin but reduced adhesion to
E-selectin by only 40%, suggesting PrMCs express other ligands for
E-selectin. PrMCs adhered strongly to tumor necrosis factor- (TNF-)-activated HUVECs, whereas adhesion to
interleukin 4 (IL-4)-activated HUVECs was lower. PrMC adhesion to
IL-4-activated HUVECs was totally 4-integrin- and
VCAM-1-dependent. Adhesion to TNF--activated HUVECs was
blocked by 50% by mAbs against 4-integrin, vascular cell
adhesion molecule-1 (VCAM-1), E-selectin, or PSGL-1, whereas
combinations of mAbs to 4-integrin plus PSGL-1, or VCAM-1 plus E-selectin, blocked adhesion by greater than 70%.
Thus, PrMCs derived in vitro predominantly use
4-integrin, VCAM-1, PSGL-1, and other ligands that bind
E-selectin for adhesion to cytokine-activated HUVEC monolayers.
These observations may explain the abundance of MCs at sites of mucosal
inflammation, where VCAM-1 and E-selectin are important inducible receptors.
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