Candidiasis in autoimmune polyendocrine syndrome-1 is due to antibodies against which target?

In autoimmune polyendocrine syndrome type 1 (APS1), individuals often develop candidiasis, which is primarily due to an impaired immune response to fungal infections. The autoimmune response in APS1 can include the production of antibodies against certain key immune mediators.

The correct choice identifies that candidiasis in this syndrome is related to antibodies against IL-17 and IL-22. These interleukins play crucial roles in the host defense against extracellular pathogens, including Candida species. IL-17 is involved in the recruitment of neutrophils to the site of infection and promotes the production of antimicrobial peptides, while IL-22 enhances epithelial responses that are protective against yeast infections. In patients with APS1, deficiencies or antibodies directed against these cytokines lead to a reduced ability to effectively combat Candida infections, resulting in an increased susceptibility to candidiasis.

This fundamental understanding of the immune response highlights the importance of IL-17 and IL-22 in maintaining mucosal immunity and fighting off fungal infections, which is why the identification of antibodies against these interleukins is directly tied to the occurrence of candidiasis in patients with autoimmune polyendocrine syndrome type 1.