The recently reported observations of Correia and Delgado1 add convincing support to other reports2,3 that an abnormal T-cell response is involved in the pathogenesis of toxic epidermal necrolysis (TEN). The observations that support the theory of immune system mediation of this disease include the following:
The occurrence of TEN as a manifestation of severe acute graft-vs-host disease suggests a cell-mediated immune pathogenesis.
The dermal infiltrate in TEN is composed mainly of activated T lymphocytes with a predominantly cytotoxic phenotype.
Patients who suffer a second bout of TEN caused by the same drug undergo a shorter incubation period and have more severe disease.
Keratinocytes express HLA-DR and ICAM-14 molecules; normally, they do not.
Recently, in the early lesions of TEN, perforin mRNA has been found in the granules of CD8 cytotoxic T cells.5
In view of these facts, it has been unfortunate that in the
Moncada B, Delgado C, Quevedo ME, Lorincz AL. Abnormal T-Cell Response in Toxic Epidermal Necrolysis. Arch Dermatol. 1994;130(1):116. doi:10.1001/archderm.1994.01690010122026