Immune Checkpoint Inhibitor–Induced Lichenoid Skin Disease: Diagnosis, Histology, and Treatment

Conclusions

• Checkpoint inhibitor–associated lichenoid skin toxicity is a common and likely increasingly recognized immune-related adverse event, especially because it often affects the skin and mucosa.
• The diagnosis cannot be made reliably from timing alone, because lichenoid eruptions can appear early, late, or even after immunotherapy has stopped.
• ICI-related lichenoid disease is clinically heterogeneous and can overlap with or evolve into other cutaneous toxicities such as psoriasis, bullous pemphigoid, or eruptive squamous proliferations.
• Histology often resembles classic lichen planus but frequently shows mixed features such as spongiosis, eosinophils, periadnexal inflammation, and atypical T-cell patterns that make the entity distinct from spontaneous lichen planus.
• The underlying immune profile is mixed rather than purely Th1-driven, with evidence for Th17, Th2, myeloid, and even B-cell involvement in different studies.
• Management usually starts with topical steroids or calcineurin inhibitors, with phototherapy and selected systemic agents used when needed, but treatment should be coordinated closely with oncology.
• Steroid-sparing approaches such as acitretin, hydroxychloroquine, methotrexate, and especially dupilumab may be useful in selected patients, while systemic prednisone is generally less favored because of worse outcomes.
• Lichenoid cutaneous reactions may correlate with better cancer outcomes, so they can carry a clinical ‘silver lining’ even when the skin disease is severe or symptomatic.