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Prepublished online as a Blood First Edition Paper on August 22, 2002; DOI 10.1182/blood-2002-05-1452.
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Blood, 15 January 2003, Vol. 101, No. 2, pp. 771-778
TRANSPLANTATION
In vitro adherence of lymphocytes to dermal endothelium under
shear stress: implications in pathobiology and steroid therapy of acute
cutaneous GVHD
Robert Sackstein,
Jane L. Messina, and
Gerald J. Elfenbein
From the Harvard Skin Disease Research Center, Harvard
Medical School, Department of Dermatology, Brigham and Women's
Hospital, and Department of Medicine, Massachusetts General Hospital,
Boston, MA; Department of Pathology and Laboratory Medicine, University
of South Florida College of Medicine, Tampa; and Department of
Oncology, Roger Williams Hospital, Providence, RI.
The extravasation of leukocytes at sites of inflammation critically
depends on initial shear-resistant adhesive interactions between
leukocytes in blood flow and target tissue endothelium. Dermal
lymphocytic infiltrates are a hallmark feature of acute cutaneous
graft-versus-host disease (acGVHD) following allogeneic hematopoietic
stem cell (allo-HSC) transplantation. These infiltrates occur commonly during periods of profound lymphopenia, suggesting that the dermal endothelial adhesive mechanism(s) promoting lymphocyte emigration in acGVHD are highly efficient. To examine this issue, we
performed Stamper-Woodruff assays on frozen sections of biopsy specimens of cutaneous lesions occurring within 100 days of HSC transplantation in 22 autologous hematopoietic stem cell transplant (auto-HSCT) and 25 allo-HSCT recipients. By using this shear-based assay, we observed lymphocyte adherence to papillary dermal vascular structures in all punch biopsy specimens of allo-HSCT recipients who
had clinicohistologic evidence of acGVHD and who were not receiving
steroids, whereas no lymphocyte adherence was observed within skin
specimens from allo-HSCT recipients who did not develop acGVHD. Within
the group of auto-HSCT recipients, 2 of 22 skin biopsies demonstrated
lymphocyte binding to dermal vessels. Among allo-HSCT patients
receiving steroid therapy for acGVHD, lymphocyte binding to dermal
endothelium was abrogated prior to resolution of rash in those who
responded, yet binding was persistent in skin from one patient whose
rash did not respond to steroid therapy. Collectively, these data
indicate that the papillary endothelium of skin in acGVHD displays
heightened capacity to support lymphocyte adhesion under shear stress
conditions and suggest that down-modulation of this endothelial
adhesive capability may be one mechanism by which steroids abrogate
acGVHD reactions.
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