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Dermal dendrocytes participate in the cellular pathology of experimental acute graft‐versus‐host disease
Author(s) -
Yoo Young H.,
Park Bong S.,
WhitakerMenezes Diana,
Korngold Robert,
Murphy George F.
Publication year - 1998
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.1600-0560.1998.tb01769.x
Subject(s) - factor xiiia , dermis , pathology , pathogenesis , graft versus host disease , antigen , disease , cd8 , immunohistochemistry , pathophysiology , medicine , immunology , biology
In a well established murine model relevant to human disease, graft‐versus‐host disease results from recognition of recipient minor histocompatibility antigens by donor bone marrow‐derived T lymphocytes. Previous studies suggest that factor XIIIa‐positive dermal dondrocytes may be involved in the pathogenesis of disorders involving antigen presentation to T cells and dermal fibrosis. This study was undertaken to determine (i) whether normal murine skin contains factor XIIIa‐positive dermal dendrocytes, and (ii) whether such cells participate in the pathophysiology of acute graft‐versus‐host disease. Graft‐versus‐host disease was produced using B10.BR CD8+ donor T cells administered to CBA recipients. Skin samples were collected weekly for a 5‐week period and evaluated by immunohistochemistry and electron microscopy. Our data indicate that normal murine dermis contains factor XIIIa‐positive cells localized primarily around deep dermal microvessels. Ultrastructural analyses reveal these cells to have long processes, pinocytotic vesicles, fibronexuses, and intimate associations with mast cells. During graft‐versus‐host disease, factor XIIIa‐positive dendrocytes appeared within the superficial dermis. By ultrastructure, the dendrocytes were hypertrophic and highly branched, and demonstrated an intimate relationship with neighboring cells. In conclusion, factor XIIIa‐positive dendrocytes comprise a normal component of the murine dermis and undergo alterations in experimental acute graft‐versus‐host disease consistent with participation in disease pathophysiology.