Reduced induction of human β-defensins is involved in the pathological mechanism of cutaneous adverse effects caused by epidermal growth factor receptor monoclonal antibodies.
R OmmoriY NakamuraFumi MiyagawaC ShobatakeK OgawaF KoyamaM ShoI OtaT KitaharaS HontsuS MuroHideo AsadaPublished in: Clinical and experimental dermatology (2020)
Epidermal growth factor receptor inhibitors (EGFRIs) frequently cause cutaneous adverse effects such as papulopustular eruptions. However, the mechanism of the reactions remains unclear. To assess the pathological mechanism of cutaneous adverse reactions caused by EGFRIs, we investigated whether EGFRIs have an influence on the innate immune response of the skin. Levels of human β-defensins (hBDs), which serve as the first line of defence against infection by pathogenic microorganisms, in the stratum corneum samples of patients treated with EGFR. monoclonal antibodies were measured before and after starting therapy. There were no obvious trends in hBD production in patients without eruptions, whereas a significant decrease in hBD1 and hBD3 production and a nonsignficant decrease in hBD2 production were observed in patients who developed papulopustular eruptions. Our results suggest that a reduction in hBD contributes to the increased incidence of papulopustular eruptions.
Keyphrases
- epidermal growth factor receptor
- immune response
- tyrosine kinase
- advanced non small cell lung cancer
- endothelial cells
- end stage renal disease
- induced pluripotent stem cells
- ejection fraction
- newly diagnosed
- chronic kidney disease
- pluripotent stem cells
- small cell lung cancer
- risk factors
- prognostic factors
- emergency department
- toll like receptor
- patient reported outcomes
- inflammatory response
- high speed