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Amy Beth Koff, MD
Department of Dermatology Baylor College of Medicine One Baylor Plaza Houston, TX 77030

Arch Dermatol. 1992;128(7):991.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 .

One possible explanation for these divergent findings . . . [Full Text PDF of this Article]

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