Polymorphic light eruption (PMLE) is the most common photodermatosis. Its pathomechanism involves:

• A Type I hypersensitivity to UV-modified skin proteins
• B Delayed-type (Type IV) hypersensitivity to a UV-induced photoantigen in the skin ✓
• C Phototoxic reaction from excess endogenous porphyrins
• D Immune complex deposition triggered by UV light in photosensitive individuals

Explanation

PMLE is a delayed-type (Type IV/cell-mediated) hypersensitivity reaction to a UV-induced (photo)antigen in the skin. UV radiation, primarily UVA, modifies cutaneous proteins to create neoantigens that are recognized by sensitized T-lymphocytes, producing the delayed (hours to days) papular, vesicular, or plaque-like eruption on UV-exposed areas. This is in contrast to solar urticaria (Type I/IgE-mediated) and porphyria (endogenous photosensitizer). Interestingly, PMLE patients show 'hardening' (immunological tolerance induction) with repeated UV exposure over summer.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.