Introduction: Interleukin 17A (IL-17A) is a pro-inflammatory cytokine produced by helper T cells (Th17) and other cells of the immune system and exerts pleiotropic effects on multiple cell lines. The role of IL-17 in the pathogenesis of numerous inflammatory disorders is well-documented. IL-17 activates signaling through the IL-17 receptor, which induces other proinflammatory cytokines, antimicrobial peptides, and neutrophil chemokines that are important for antifungal activity.
Evidence acquisition: Healthy levels of IL-17 can protect the host against extracellular bacterial and fungal infections in mucous membranes and epithelia. IL-17 deficiency reduces control of certain infections, while excessive IL-17 can produce unwanted inflammatory effects.
Evidence synthesis: Although the efficacy of the therapeutic blockade of this cytokine has been proven in several autoimmune diseases such as psoriasis and psoriatic arthritis, this strategy could also exacerbate fungal infections in such patients. Therefore, a better understanding of IL-17-mediated immunity to Candida is necessary for the development of autoimmune therapeutics that maintain antifungal immunity.
Conclusions: In this review, we include a study of the new anti-IL-17 biological agents (secukinumab, ixekizumab, and bromalizumab) used for moderate-to-severe psoriasis and psoriatic arthritis treatment in clinical practice, as well as pivotal trials with bimekizumab. We study the relationship of these biological agents and the appearance of candidiasis in its various clinical forms.