In acute skin injury, healing is significantly impaired by excessive release of ROS (Li et al, 2007). Melanin, an efficient scavenger of radical species in the skin, performs a key, natural role in ROS scavenging in response to UVR and is upregulated in response to toxic insult. Known as an absorber of light, lending pigmentation to our skin, melanin is produced by melanocytes and transferred to keratinocytes, where the electronic and molecular structure of melanin leads to its performance as a scavenger of radicals, trapping destructive species.

We read with interest the report of Zeng et al (2024) that provides insight into the mechanism(s) whereby skin colonization by Staphylococcal aureus plays a key role in progression of cutaneous T-cell lymphoma (CTCL). S aureus is known to produce >20 enterotoxins (so called superantigens) that crosslink major histocompatibility complex (MHC) class II molecules on the surface of antigen-presenting cells with the beta chain of the TCR in the skin and elsewhere. This MHC–T-cell cross-linking activates T cells irrespective of any antigen presentation, to release cytokines such as IFN-γ (Tuffs et al, 2022).