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Mycology
An International Journal on Fungal Biology
Volume 15, 2024 - Issue 1: Pathogenic Fungi and Health
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Review

Risk of candidiasis associated with interleukin-17 inhibitors: Implications and management

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Pages 30-44 | Received 07 Jun 2023, Accepted 27 Sep 2023, Published online: 20 Oct 2023

Figures & data

Figure 1. Model of oral candidiasis and the immune system’s response for clearing Candida species. In response to Candida species, macrophages are activated, which recruit CD4+T cells or TH17 cells through various cytokines, in order to activate neutrophils or release β-defensin to clear Candida infection.

Figure 1. Model of oral candidiasis and the immune system’s response for clearing Candida species. In response to Candida species, macrophages are activated, which recruit CD4+T cells or TH17 cells through various cytokines, in order to activate neutrophils or release β-defensin to clear Candida infection.

Figure 2. IL-17 inhibitors, attachment sites, and mechanism of action. Secukinumab and ixekizumab interact with IL-17A/A, and A/F, bimekizumab attached to IL-17A/A, A/F, and F/F, and brodalumab inhibit IL-17A, IL-17C, and IL-17E.

Figure 2. IL-17 inhibitors, attachment sites, and mechanism of action. Secukinumab and ixekizumab interact with IL-17A/A, and A/F, bimekizumab attached to IL-17A/A, A/F, and F/F, and brodalumab inhibit IL-17A, IL-17C, and IL-17E.

Figure 3. Monitoring of candidiasis in patients treated with IL-17 inhibitors.

Figure 3. Monitoring of candidiasis in patients treated with IL-17 inhibitors.

Figure 4. Clinical presentation, diagnosis and treatment of candidiasis associated with IL-17 inhibitors.

Figure 4. Clinical presentation, diagnosis and treatment of candidiasis associated with IL-17 inhibitors.