To the Editor.—
In the January 1992 issue of the Archives, Villada et al1 discussed the immunopathology of toxic epidermal necrolysis (TEN). The authors described the dermal infiltrate in TEN as consisting primarily of activated T-helper cells. They also noted abnormal expression of HLA-DR antigens by keratinocytes, which they postulate may be secondary to interferon gamma. Their findings starkly contrast with the results of Heng and Allen2 who described the immunopathologic infiltrate of TEN in the November 1991 issue of the Journal of the American Academy of Dermatology.Using similar techniques, Heng and Allen found the infiltrate populated with suppressor T lymphocytes and proposed T-lymphocyte—mediated cytolysis as a mechanism in TEN, analogous to graft-vs-host disease. Heng and Allen, like Villada et al, found aberrant expression of HLA-DR by keratinocytes but suggested that this was related to tumor necrosis factor α.One possible explanation for these divergent findings
Koff AB. Two Divergent Findings in TEN. Arch Dermatol. 1992;128(7):991. doi:10.1001/archderm.1992.01680170127023
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