Lymphocyte subsets and Langerhans' cells in toxic epidermal necrolysis. Report of a case

Uncovering Histologic Criteria With Prognostic Significance in Toxic Epidermal Necrolysis

“…20,21 A correlation was drawn between TEN and other cytotoxic skin disorders; however, it was suggested that epidermal damage in TEN might be due in part to nonantibody circulating lymphokines as an explanation for the "paucity" of dermal inflammation. Paquet and Pierard 22 showed that TEN is characterized immunopathologically by an increased ratio of dermal dendrocytes to dermal lymphocytes, in contrast to the opposite pattern seen in EM where lymphocytes predominate.…”

Numerical, morphological and phenotypic changes in Langerhans cells in the course of murine graft-versus-host disease

“…Graft‐versus‐host disease (GVHD) and some diseases that histologically mimic GVHD, such as toxic epidermal necrolysis (TEN) and Stevens–Johnson syndrome (SJS), demonstrate clinical, histological and immunopathophysiological features in common 1–3 . Skin is one of the most frequently involved organs in these diseases 4,5 .…”

“…showed that LCs were more severely depleted in mice that developed GVHD following TBI and bone marrow transplantation than in mice that received TBI alone 13 . Furthermore, in post‐transfusion GVHD or other diseases with similar histological changes to GVHD, LCs are depleted from the epidermis even in the absence of conditioning regimens 3,16 , 17,21 . Accordingly, factors other than conditioning regimens, which are common to post‐transplantation GVHD and these diseases, may reduce epidermal LCs.…”

“…The basic mechanism of the epidermal cell (EC) injury has been reported to be apoptosis from an attack by alloreactive or autoreactive T cells 8–10 . It is also known that the number of epidermal Langerhans cells (LCs) is reduced in the disease course 3,11–17 . It has been proposed that LC depletion in post‐transplantation GVHD is mainly due to conditioning regimens such as total body irradiation (TBI) and chemotherapy 14,15 .…”

Would Cyclosporin A Be Beneficial to Mitigate Drug-Induced Toxic Epidermal Necrolysis?

“…Immunohistological studies have recently shed some light on the biological factors. An active role has been ascribed to T lymphocytes, particularly CD4+ cells in the dermis and CD8+ cells in the epidermis [18, 19, 20, 21]. L1-protein-rich macrophages and factor-XIIIa-positive dendrocytes appear to have significant pathogenic roles in the epidermis and dermis, respectively [22].…”