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Dermal dendrocytes participate in the cellular pathology of experimental acute graft-versus-host disease
Y H Yoo1, B S Park, D Whitaker-Menezes
1Department of Anatomy and Cell Biology, Dong-A University College of Medicine, Pusan, South Korea. yhyoo@daunet.donga.ac.kr
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 dendrocytes 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.
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 dendrocytes 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.