Salomé LeibundGut‐Landmann

This study shows that Malassezia furfur hyphal growth depends on mating-type loci and is promoted by host skin lipids, linking parasexual reproduction to pathogenic traits.

This study uses FTIR spectroscopy and WGS to show increased strain diversity of Malassezia pachydermatis in dogs with atopic dermatitis, with specific phylogroups enriched in affected animals.

The paper identifies a novel macrophage-like population in exocrine glands sustained by ILC2-derived GM-CSF, showing conservation across species.

This study identifies a novel Clec7a-KLR axis that regulates DC function and CD4 T cell responses, linking innate and adaptive immunity in host defense and inflammation.

This paper identifies KLRE1 as a regulator of dendritic cell and T cell activation through heterodimeric interactions with KLRI1 and KLRI2, influencing immune outcomes during fungal infection.

This study identifies Tsa1b as a virulence factor in Candida auris that enhances oxidative stress resistance and infection progression.

This study uses Fourier transform infrared spectroscopy to rapidly distinguish Malassezia species and resolve strain-level typing in M. pachydermatis, matching whole-genome sequencing results.

This study shows that altering BRG1 and CYR1 in a low-virulence C. albicans strain does not increase its virulence in vivo, suggesting complex gene networks regulate fungal pathogenicity.

This study shows that Mgl2+ cDC2s trigger fungal allergic inflammation through a glycolytic shift driven by glucose availability after spore uptake.

This study shows Malassezia promotes skin homeostasis by producing tryptophan metabolites that activate AhR, enhancing barrier function and reducing inflammation.

The paper investigates how Card9 and MyD88 regulate Th17 immunity against Malassezia in murine skin, showing Dectin-2's role in Th17 activation and MyD88's involvement in T cell-intrinsic signaling.

This study identifies the Rim/Pal pathway in Malassezia sympodialis as essential for alkaline pH adaptation and demonstrates its role in atopic dermatitis.

This study shows that impaired skin barriers in atopic dermatitis allow Malassezia yeast to grow more efficiently due to changes in the skin's lipid environment.

This study identifies Vγ4+ γδ T cells as key mediators of IL-17-dependent fungal control against Malassezia in skin, showing memory-like responses and direct recognition of fungal ligands.