Corticosteroids drive oral candidiasis by impairing type-17 immunity without inducing interferon-gammopathy.

Corticosteroids cause oral candidiasis primarily by impairing type-17 immunity, not through interferon-gamma-driven inflammation, in a widely used mouse model.

• Why it matters: Understanding the specific immune pathways affected by corticosteroids is crucial for developing targeted treatments and preventing opportunistic infections like oral candidiasis in patients receiving these drugs.
• What they did: The study used the cortisone acetate mouse model to investigate immune responses, revealing that corticosteroid susceptibility is mainly due to suppression of type-17 immunity, while interferon-gamma pathways are not involved.
• The result: Findings establish that loss of type-17 immunity is the key driver of corticosteroid-induced oral candidiasis, enabling more precise therapeutic strategies to bolster mucosal immunity and reduce infection risk.