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Elevated NLRP1 and IL-1β Expression Supports Inflammasome Activation in SJS/TEN.

Created on 18 Jun 2026

Authors

Merve Kaya, Burak Celik, Kübra Katipoglu, Funda Erduran, Mehmet Ali Dogan, Nuran Süngü

Published in

Journal of cutaneous pathology. Jun 18, 2026. Epub Jun 18, 2026.

Abstract

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare, life-threatening mucocutaneous reactions most commonly triggered by medications. While cytotoxic T-cell-mediated keratinocyte death is considered central to disease pathogenesis, the contribution of innate immune pathways, particularly NLRP1-mediated inflammasome activation, remains insufficiently characterized.
In this retrospective study, we analyzed skin biopsy specimens from 22 patients with histopathologically confirmed SJS/TEN and 18 controls with normal skin. Immunohistochemical staining for NLRP1 and IL-1β was semiquantitatively assessed using H-scores, and clinical features including suspected triggers, SCORTEN, and outcomes were recorded.
NLRP1 and IL-1β expression in both epidermal keratinocytes and dermal lymphocytes was significantly elevated in SJS/TEN compared with controls (all p < 0.05), and NLRP1 levels demonstrated a strong positive correlation with SCORTEN (p < 0.001). No significant differences in expression were observed between survivors and non-survivors.
These findings support a role for inflammasome activation in SJS/TEN pathogenesis and suggest that NLRP1 may serve as a potential biomarker of disease severity. Larger, prospective studies are warranted to confirm these observations.

PMID:
42312938
Bibliographic data and abstract were imported from PubMed on 18 Jun 2026.

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