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Updated: Sep 12, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Type 2 immunity links eczematous and lichenoid eruptions caused by immune checkpoint inhibitors
Marjan Azin1, Parisa Farokh1, Alexander McGarry1
1Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
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.
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