REAPPRAISAL OF HISTOLOGIC FEATURES OF THE ACUTE CUTANEOUS GRAFT-VERSUS-HOST REACTION-BASED ON AN ALLOGENEIC RODENT MODEL

Citation
Td. Horn et al., REAPPRAISAL OF HISTOLOGIC FEATURES OF THE ACUTE CUTANEOUS GRAFT-VERSUS-HOST REACTION-BASED ON AN ALLOGENEIC RODENT MODEL, Journal of investigative dermatology, 103(2), 1994, pp. 206-210
Citations number
18
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
0022202X
Volume
103
Issue
2
Year of publication
1994
Pages
206 - 210
Database
ISI
SICI code
0022-202X(1994)103:2<206:ROHFOT>2.0.ZU;2-Y
Abstract
We employed a rat model of complete major histocompatibility complex-m ismatched allogeneic bone marrow transplantation to better characteriz e the histologic expression of the acute cutaneous graft-versus-host r eaction (GVHR), compared with changes due to the preparative regimen. Cyclosporin A abolished the development of this GVHR. Low levels of dy skeratotic cells were present in all groups (allogeneic and syngeneic transplants with and without cyclosporin A) and, alone, were insuffici ent to diagnose a cutaneous GVHR. A consistent histologic feature of t he GVHR was significant lymphoid infiltration of the dermis. The patte rn of cytotoxic folliculitis involved follicular epithelium above the entry of sebaceous glands. Immunostain for major histocompatability co mplex class II, IA, and IE antigens revealed that dendritic cells with in the follicle were limited to this upper region and that lower folli cular epithelium did not upregulate expression with evolution of the G VHR. Based on this model,we conclude 1) that the diagnostic scheme for the acute cutaneous GVHR should include lymphoid infiltration of the dermis, 2) that the preparative regimen (including total body irradiat ion) induces persistent low levels of dyskeratotic cells (two to three cells/linear mm of epidermis), and 3) that the pattern of follicular involvement may relate to the distribution of dendritic cells and to a n inability of lower follicular epithelium to upregulate major histoco mpatability complex class II antigens.