{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T19:48:42Z","timestamp":1791402522332,"version":"4.3.3"},"reference-count":61,"publisher":"American Society of Hematology","issue":"8","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>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 \u03b14\u03b21, low levels of \u03b27, and the \u03b22-integrins \u03b1L\u03b22 and \u03b1M\u03b22. 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\u2013PSGL-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-\u03b1 (TNF-\u03b1)\u2013activated HUVECs, whereas adhesion to interleukin 4 (IL-4)\u2013activated HUVECs was lower. PrMC adhesion to IL-4\u2013activated HUVECs was totally \u03b14-integrin\u2013 and VCAM-1\u2013dependent. Adhesion to TNF-\u03b1\u2013activated HUVECs was blocked by 50% by mAbs against \u03b14-integrin, vascular cell adhesion molecule\u20131 (VCAM-1), E-selectin, or PSGL-1, whereas combinations of mAbs to \u03b14-integrin plus PSGL-1, or VCAM-1 plus E-selectin, blocked adhesion by greater than 70%. Thus, PrMCs derived in vitro predominantly use \u03b14-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.<\/jats:p>","DOI":"10.1182\/blood.v99.8.2890","type":"journal-article","created":{"date-parts":[[2002,10,11]],"date-time":"2002-10-11T18:33:52Z","timestamp":1034361232000},"page":"2890-2896","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":40,"title":["Human mast cell progenitors use \u03b14-integrin, VCAM-1, and PSGL-1 E-selectin for adhesive interactions with human vascular endothelium under flow conditions"],"prefix":"10.1182","volume":"99","author":[{"given":"Joshua A.","family":"Boyce","sequence":"first","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth A.","family":"Mellor","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandy","family":"Perkins","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaw-Chyn","family":"Lim","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francis W.","family":"Luscinskas","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2020021223214740900_B1","doi-asserted-by":"crossref","first-page":"75","DOI":"10.1038\/381075a0","article-title":"Critical protective role of mast cells in a model of acute septic 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