Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis
- 1 April 1996
- journal article
- Published by Oxford University Press (OUP) in British Journal of Dermatology
- Vol. 134 (4) , 710-714
- https://doi.org/10.1111/j.1365-2133.1996.tb06976.x
Abstract
Summary Toxic epidermal necrolysis (TEN) and Stevens‐Johnson syndrome (SJS) are life‐threatening diseases characterized by extensive epidermal destruction. The aim of our study was to investigate apoptosis in keratinocytes of patients with TEN and TEN/SJS overlap syndrome. Keratinocytes from TEN patients were found to undergo extensive apoptosis. These results suggest that cell destruction in TEN occurs as a result of apoptosis. Our findings suggest that apoptosis inhibitory agents may play an important part in the therapeutic strategy of TEN.Keywords
This publication has 22 references indexed in Scilit:
- Pharmacological inhibition of programmed lymphocyte deathImmunology Today, 1994
- Programmed cell death, apoptosis and killer genesImmunology Today, 1993
- Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.The Journal of cell biology, 1992
- Social controls on cell survival and cell deathNature, 1992
- Immunopathology of toxic epidermal necrolysis. Keratinocytes, HLA-DR expression, Langerhans cells, and mononuclear cells: an immunopathologic study of five casesArchives of Dermatology, 1992
- Apoptosis And Programmed Cell Death In ImmunityAnnual Review of Immunology, 1992
- Programmed Cell Death in Terminally Differentiating Keratinocytes: Role of Endogenous EndonucleaseJournal of Investigative Dermatology, 1991
- T-cell subsets in drug-induced toxic epidermal necrolysis. Possible pathogenic mechanism induced by CD8-positive T cellsArchives of Dermatology, 1991
- Toxic epidermal necrolysis (Lyell syndrome)Journal of the American Academy of Dermatology, 1990
- Antibodies to CD3/T-cell receptor complex induce death by apoptosis in immature T cells in thymic culturesNature, 1989