Journal of cutaneous pathology · 2026
Elevated NLRP1 and IL-1β Expression Supports Inflammasome Activation in SJS/TEN.
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Kaya Merve, Celik Burak, Katipoglu Kübra, Erduran Funda, Dogan Mehmet Ali, Süngü Nuran
Аннотация
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.