Study identifies harmful immune response to Candida albicans in Crohn's disease

A research team from the Excellence Cluster “Precision Medicine in Chronic Inflammation” (PMI) at Kiel University has published a new study in *Immunity* that clarifies the role of Th17 cells in the body’s defense against the common yeast *Candida albicans*. The fungus is normally present on mucous membranes such as the oral cavity and intestines, where it is kept in check by the immune system. The study, released today, systematically details how these specialized T helper cells function in a healthy host, where they originate, and how they can become pathogenic in the context of Crohn’s disease.

The investigators found that Th17 cells are produced early in life and are trained by the immune system to recognize and limit *Candida* colonization. In a healthy state, these cells release cytokines that strengthen mucosal barriers and recruit other immune cells to prevent fungal overgrowth. However, the study shows that in individuals with Crohn’s disease, the regulatory pathways that normally restrain Th17 activity are disrupted, allowing these cells to over‑activate and contribute to intestinal inflammation. The research maps the cellular origins of Th17 cells and identifies key signaling molecules that switch their protective role into a harmful one.

These findings provide a clearer picture of the dual nature of Th17 cells and highlight potential therapeutic targets for treating Crohn’s disease. By pinpointing the mechanisms that lead to their dysregulation, the study opens avenues for interventions that could restore the balance of the immune response to *Candida* without compromising overall mucosal health.