Abstract

The link between actinic keratosis (AK), squamous cell carcinoma (SCC), and a fully functional immune system has been frequently observed but is poorly understood. Elderly and immunosuppressed individuals and those with weakened immune systems caused by disease are all at increased risk of developing AK and/or SCC. This risk is particularly enhanced at sites that receive high levels of ultraviolet exposure from the sun, which is thought to be a driver of DNA mutations in the skin. The immune system appears to play a key role in preventing these mutations from progressing to malignant disease. AK is often considered to be a pre-cancerous lesion that may develop into SCC. However, the vast majority of AKs, in contrast to SCCs, regress naturally or in response to immune-modifying medications. The cellular mechanisms involved in this immune-based process remain elusive and raise the following question: does the immune make-up or immune functionality within AK differ fundamentally from that within SCC? This chapter will outline the skin as a site of considerable immunological activity, highlight the consequences of dysregulated immune activity in the skin, and discuss what little we know of immune infiltrates and their associated functions within AK and SCC.

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