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Updated: Jul 11, 2026

Murine Full-thickness Skin Transplantation
Published on: January 2, 2017
Clinicopathologic studies on human epithelial autografts and allografts
1Department of Plastic and Reconstructive Surgery, Hokkaido University School of Medicine, Japan.
Insights
Cultured epithelial allografts were rejected in skin graft donor sites, unlike permanent autografts. Host Langerhans-like cells appear to play a key role in this immune rejection process.
Area of Science:
- Immunology
- Dermatology
- Transplantation Biology
Background:
- Split-thickness skin grafting is a common procedure.
- Graft survival depends on immune compatibility.
- The role of Langerhans cells in graft rejection is not fully understood.
Purpose of the Study:
- To compare the survival and immune response of cultured epithelial allografts versus autografts.
- To investigate the role of Langerhans cells in epithelial graft rejection.
Main Methods:
- Comparison of cultured epithelial allografts and autografts on donor sites.
- Immunohistochemical and electron microscopic examination of grafts.
- Assessment of graft survival, rejection signs, and cell infiltration.
Main Results:
- Autografts survived permanently without rejection.
- Allografts showed signs of rejection by week 2 and were reepithelialized by host by week 3.
- Host Langerhans-like cells infiltrated allografts extensively, while scarce in autografts.
Conclusions:
- Cultured epithelial allografts are immunologically rejected.
- Host Langerhans-like cells are implicated in the rejection of epithelial allografts.
- Understanding these mechanisms can improve skin grafting outcomes.
Abstract:
We compared the survival of cultured epithelial allografts and epithelial autografts applied to donor sites for split-thickness skin grafts. Before grafting, cultured epithelium was devoid of Langerhans cells (LCs) or lymphoid cells by immunohistochemical and electron microscopic examinations. The autografts attached to the wounds permanently, without any clinical evidence of rejection. In contrast, allografts, which were mismatched for MHC and blood-type antigens, appeared to adhere firmly only until day 7. By the second week, signs of graft rejection were apparent: The graft changed color, and the underlying dermis underwent "microerosion" and denudation. By the third week, the area formerly occupied by the allograft had the same coloration as ungrafted wounds and apparently had undergone reepithelialization by the host. Immunohistochemical and ultrastructural studies clearly demonstrated that host Langerhans-like cells (without Birbeck granules) appeared in both autografts and allografts. However, these cells were numerous and distributed widely throughout allografts, whereas they were scarce and confined to the basal layer of autografts. Typical Langerhans cells (containing Birbeck granules) were present in the prickle-cell layer of autografts by day 7. The present study strongly indicates that allografts of cultured epithelium are rejected. Furthermore, given the known ability of Langerhans-like cells to function as accessory cells in T-cell activation, our results point to a role for host Langerhans-like cells in immunologically mediated rejection of the epithelial allografts.
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