# Host–Candida auris interactions in the skin

## TL;DR

This paper reviews how Candida auris interacts with the skin, focusing on factors that allow it to colonize and cause infections.

## Contribution

The paper provides a comprehensive overview of host and fungal factors involved in C. auris skin colonization and infection.

## Key findings

- C. auris has a unique mannan outer layer and adhesins that aid in skin colonization.
- Host immune responses, including IL-17 and IFN-γ, influence the outcome of C. auris infection.
- Excessive IFN-γ responses contribute to epithelial pathology and fungal persistence.

## Abstract

Candida auris is an emerging, multidrug-resistant fungal pathogen that causes healthcare-associated outbreaks and life-threatening systemic infections. Unlike other Candida species, C. auris exhibits a distinct capacity for persistent skin colonization. In this review, we summarize our current understanding of clinical risk factors and host-microbe interactions that underlie C. auris skin colonization and infection. We discuss fungal determinants, including the unique mannan outer layer, fungal adhesins, the protein kinase Hog1, and other pathways in C. auris that govern adaptation in the skin. Furthermore, we highlight host immune mechanisms, including cytokine mediators (IL-1Ra, IL-17) and innate immune cells (neutrophils, macrophages, innate lymphocytes), that shape the outcome of C. auris skin colonization and infection. We also discuss how excessive IFN-γ responses drive epithelial pathology at the cutaneous barrier and enhance fungal persistence. Finally, we outline emerging research directions to understand host and microbe factors governing long-term colonization, with implications for developing novel therapeutic and vaccine strategies against this skin-tropic, multidrug-resistant fungal pathogen.