Immunopathology of Toxic Epidermal Necrolysis

Villada, Gabriel

doi:10.1001/archderm.1992.01680110060006

Cited by 80 publications

(20 citation statements)

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“…Cell-mediated cytotoxicity has been suggested by infiltration of inflammatory cells in areas of epidermal necrolysis [20,21]. Among these ceils, monocytes/macrophages and T-cell lymphocytes infiltrating dermis and epidermis could play a crucial role via local TNFa and cytotoxic secretion [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary complications in toxic epidermal necrolysis: a prospective clinical study

et al. 1997

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"Specific" involvement of bronchial epithelium was noted in 27% of cases and must be suspected when dyspnea, bronchial hypersecretion, normal chest X-ray, and marked hypoxemia are present during the early stages of toxic epidermal necrosis. Bronchial injury seems to indicate a poor prognosis, as mechanical ventilation was required for most of these patients and was associated with a high mortality.

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Section: Discussionmentioning

confidence: 99%

Pulmonary complications in toxic epidermal necrolysis: a prospective clinical study

et al. 1997

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“…Cells from CBZ-hypersensitive patients have been shown to produce variable but occasionally high levels of IFN-␥ and IL-5 (Koga et al, 2000;Leyva et al, 2000;Villada et al, 1992;Mauri-Hellweg et al, 1995;Schnyder et al, 1998), which is consistent with the pathophysiology of the adverse reaction. However, the precise role of T cells in CBZ hypersensitivity is not known.…”

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confidence: 85%

Hypersensitivity Reactions to Carbamazepine: Characterization of the Specificity, Phenotype, and Cytokine Profile of Drug-Specific T Cell Clones

et al. 2003

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Administration of carbamazepine (CBZ) causes hypersensitivity reactions clinically characterized by skin involvement, eosinophilia, and systemic symptoms. These reactions have an immune etiology; however, the role of T cells is not well defined. The aim of this study was to characterize the specificity, phenotype, and cytokine profile of CBZ-specific T cells derived from hypersensitive individuals. Proliferation of blood lymphocytes was measured using the lymphocyte transformation test. CBZ-specific T cell clones were generated by serial dilution and characterized in terms of their cluster of differentiation and T cell receptor V␤ phenotype. Proliferation, cytotoxicity, and cytokine secretion were measured by [ 3 H]thymidine incorporation, 51 Cr release, and enzyme-linked immunosorbent assay, respectively. HLA blocking antibodies were used to study the involvement of antigen-presenting cells. The specificity of the drug T cell receptor interaction was studied using CBZ metabolites and other structurally related compounds. Lymphocytes from hypersensitive patients (stimulation index: 32.1 Ϯ 24.2 [10 g ml Ϫ1 ]) but not control patients (stimulation index: 1.2 Ϯ 0.4 [10 g ml Ϫ1 ]) proliferated upon stimulation with CBZ. Of 44 CBZ-specific T cell clones generated, 10 were selected for further analysis. All 10 clones were either CD4ϩ or CD4ϩ/ CD8ϩ, expressed the ␣␤ T cell receptor, secreted IFN-␥, and were cytotoxic. T-cell recognition of CBZ was dependent on the presence of HLA class II (DR/DQ)-matched antigen-presenting cells. The T cell receptor of certain clones could accommodate some CBZ metabolites, but no cross-reactivity was seen with other anticonvulsants or structural analogs. These studies characterize drug-specific T cells in CBZ-hypersensitive patients that are phenotypically different from T cells involved in other serious cutaneous adverse drug reactions.

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“…7 The immune reaction can be triggered by drugs or infections. 8 Genetic factors are associated with a predisposition to SJS.…”

Section: Discussionmentioning

confidence: 99%

Fluconazole-induced Stevens-Jonson syndrome

Keshri

Kumar

et al. 2014

Int J Basic Clin Pharmacol

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Immunopathology of Toxic Epidermal Necrolysis

Abstract: These findings, although not specific, are consistent with an immune cellular reaction, but they could also be linked to an inflammatory reaction initiated by epidermal damages whatever its primary mechanism.

Cited by 80 publications

References 0 publications

Pulmonary complications in toxic epidermal necrolysis: a prospective clinical study

Pulmonary complications in toxic epidermal necrolysis: a prospective clinical study

Hypersensitivity Reactions to Carbamazepine: Characterization of the Specificity, Phenotype, and Cytokine Profile of Drug-Specific T Cell Clones

Fluconazole-induced Stevens-Jonson syndrome

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