Skin Inflammation and Cancer

Chronic inflammatory skin diseases like cutaneous T-cell lymphoma (CTCL) and atopic dermatitis (AD) are driven by pathogenic CD4⁺ T cells and shaped by a complex interplay with the skin microenvironment. A shared feature of both conditions is colonisation with Staphylococcus aureus, which exacerbates disease through toxin-mediated immune activation, skin barrier damage, and resistance to therapy.

Our research explores how S. aureus modulates local immune responses and promotes treatment resistance in malignant T cells. We focus on the identification of pathogenic T-cell subsets, the role of MHC class II-expressing keratinocytes in antigen presentation, and how bacterial superantigens (SEs) drive inflammation. Recent findings show that S. aureus and its toxins can induce drug resistance in cancer cells - a process reversed by antibiotics or novel bacteriophage-derived enzymes (endolysins), highlighting their therapeutic potential.

We also investigate the clonal diversity of CTCL, revealing that genetically distinct cancer subclones with identical TCRs may respond differently to stimuli and therapy, contributing to disease persistence. These discoveries point to the need for precision medicine approaches in CTCL, including subclone-targeted treatments.

Ongoing research initiatives include the development of a novel cancer cell-targeted treatment model, characterization of S. aureus strains from CTCL and AD patients across different disease stages, investigation of bacterial regulators of virulence factors and toxins - particularly SEs - to identify potential small-molecule inhibitors, and the discovery and evaluation of new endolysins to mitigate S. aureus-mediated immune dysregulation and disease progression in AD and CTCL.