Journal of the American Academy of Dermatology · 2025
Type 2 immunity links eczematous and lichenoid eruptions caused by immune checkpoint inhibitors.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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Azin Marjan, Farokh Parisa, McGarry Alexander, Leung Bonnie W, Roster Kathleen, Rashdan Hannah, Rajeh Ahmad, Khattab Sara, Stephens Michael R, Thang Christopher Jayee, Fisher David E, Nazarian Rosalynn M, Chen Steven T, Semenov Yevgeniy R, Demehri Shadmehr
Аннотация
BACKGROUND: Cutaneous immune-related adverse events (cirAEs) induced by immune checkpoint inhibitor (ICI) therapy share clinical features with spontaneous inflammatory dermatoses. However, the exact immunopathogenesis of cirAEs remains unclear.
OBJECTIVE: To investigate the inflammation that mediates the most common cirAEs, lichenoid eruption (LE) and eczematous eruption (EE).
METHODS: In a prospective cohort study, participants with cancer on ICI therapy with any clinically visible cirAEs were enrolled. T helper-1 (Th1) and Th2 cell responses in cirAEs were compared to spontaneous lichenoid dermatitis and eczematous dermatitis.
RESULTS: Among 88 cirAE biopsies collected, LE (35.22%) and EE (31.81%) accounted for most cases. In contrast to lichenoid dermatitis, we found that the CD4+/CD8+ T-cells and Th2/Th1 ratios were increased in ICI-induced LE, similar to EE. Importantly, we identified several cirAEs displaying a combination of LE and EE on pathology.
LIMITATIONS: Only the most common types of cirAEs were evaluated, and Th17 cells were not analyzed.
CONCLUSION: Our findings indicate that LE and EE may represent a cirAE spectrum with a common underlying immunologic mechanism. Thus, understanding the immunopathogenesis of cirAEs can aid in their treatment and prevention.
OBJECTIVE: To investigate the inflammation that mediates the most common cirAEs, lichenoid eruption (LE) and eczematous eruption (EE).
METHODS: In a prospective cohort study, participants with cancer on ICI therapy with any clinically visible cirAEs were enrolled. T helper-1 (Th1) and Th2 cell responses in cirAEs were compared to spontaneous lichenoid dermatitis and eczematous dermatitis.
RESULTS: Among 88 cirAE biopsies collected, LE (35.22%) and EE (31.81%) accounted for most cases. In contrast to lichenoid dermatitis, we found that the CD4+/CD8+ T-cells and Th2/Th1 ratios were increased in ICI-induced LE, similar to EE. Importantly, we identified several cirAEs displaying a combination of LE and EE on pathology.
LIMITATIONS: Only the most common types of cirAEs were evaluated, and Th17 cells were not analyzed.
CONCLUSION: Our findings indicate that LE and EE may represent a cirAE spectrum with a common underlying immunologic mechanism. Thus, understanding the immunopathogenesis of cirAEs can aid in their treatment and prevention.