Skip to main content
. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: J Am Acad Dermatol. 2015 Sep;73(3):367–381. doi: 10.1016/j.jaad.2015.01.055

Figure 1.

Figure 1

Immune response to fungal infection. A. Pattern recognition receptors such as toll-like receptors (TLR) and C-type lectin receptors (e.g. Dectin-1) present on macrophages, dendritic cells, activate independent pathways. TLR2 and TLR4 use the adaptor protein MyD88 to activate nuclear factor kappa B (NF-κB). This transcription factor translocates into the nucleus and facilitates transcription of pro-inflammatory cytokines. Dectin-1 signals through the adaptor protein caspase recruitment domain family, member 9 (CARD-9), also activating NF-κB. Binding of interferon-γ (IFN) to its receptor on macrophages allows for homodimerization of signal transducer and activator of transcription 1 (STAT1). This transcription factor produces interferons and proinflammatory cytokines that inhibit Th17 cell development. B. Th17 cells, which produce cytokines critical for antifungal immunity, signal through STAT3. C. IL-17 receptors are expressed on numerous nonhematogenous cells. IL-17 binds its receptor allowing for activation of NF-κB through the adaptor protein ACT1, producing pro-inflammatory chemokines and cytokines that are important to the host defense against fungal organisms.