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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Biochim Biophys Acta. 2013 Apr 6;1844(1 0 0):10.1016/j.bbapap.2013.03.023. doi: 10.1016/j.bbapap.2013.03.023

Fig. 11.

Fig. 11

Host defense system against the fungus C. albicans. The response is governed by a network of cytokine (blue) and chemokine (red) production processes, that are triggered in response to the pathogen, B, which interacts with an epithelial cell (blue box surrounding B). The cell releases interleukin IL-8 which, in turn, recruits circulating neutrophils (N). Once activated by different interleukins and cytokines, such as GM-CSF and G-CSF, neutrophils produce TNFα and other cytokines and effect changes in epithelial gene transcription. CCL20 and β-defensin 2 activate dendritic cells (D) and, together with TGFβ, IL-1β and IL-6, lead to the induction of T-cell differentiation to the Th1 phenotype. CCL20 and β-defensin 2 also recruit Treg-cells that counteract the Th17 response. Finally, infected epithelial cells produce cytokines, such as IL-19, IL-20 and IL-24, which function in an autocrine fashion. Adapted from [54].