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IL-17A and IL-17F exert distinct biological effects during pulmonary infection; the IL-17F/IL-17RC signaling axis has the potential to significantly worsen pathogen-associated inflammation of the lower respiratory tract.
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our results indicate that Th17 cells contribute to the airway vascular remodeling in asthma by mediating EPC chemotaxis, as well as PMVEC tube formation, via IL-17A rather than IL-17F.
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Data indicate that IL-17A repressed IL-17F secretion in vitro and in vivo.
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The concentrations in plasma of IL-17A, IL-17F, and the IL-17AF heterodimer all were increased greatly in mice after endotoxemia.
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IL-17A and IL-17F secreted by CD4+Th17 cells specific to lung self-antigens are critical mediators of autoimmunity leading to the pathogenesis of obliterative airway disease.
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The Th17 subset of T-lymphocytes produces IL-17F to stimulate bone healing.
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IL-17F is not required for development of T helper cell (Th)2-type allergic airway inflammation.
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Together, our findings demonstrate a protective role for IL-17F in colon cancer development, possibly via inhibiting tumor angiogenesis
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These results demonstrate that IL-17A/F plays a critical role in Legionella pneumophila pneumonia, probably through induction of proinflammatory cytokines and accumulation of neutrophils at the infection site.
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CNS2 is sufficient and necessary for Il17 and optimal Il17f gene transcription in Th17 cells
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IL-17F was produced in peritoneal macrophages after TLR4 activation, peaking after 12 h. This effect was completely dependent on the presence of MyD88. The copresence of the complement activation product C5a amplified IL-17F production.
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This work demonstrates the important roles of both IL-17 signaling and neutrophils in clearing this pathogen and surviving pulmonary Bacillus anthracis infection.
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these results suggest the proinflammatory and essential role of IL-17F to develop spontaneous intestinal tumorigenesis in Apc(Min/+) mice in the presence of IL-17A.
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Data show that Mel-18 and Ezh2 positively regulate the expression of Il17a and Il17f.
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Increased resistance to infection in a mouse model of tularemia was associated with a specific increase in IL-17A/F
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IL-17A and IL-17F induce the production of chemokines MCP-1 and MIP-2 via MAPK pathways (p38 MAPK and ERK1/2), as well as mRNA transcription and protein translation and have synergistic effects with TNF-alpha and IL-1beta in cultured mesangial cells.
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Intranasal administration of adenovirus expressing IL-17F results in bronchoalveolar lavage neutrophilia and inflammatory gene expression in the lung.
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a role for IL-17F in the induction of neutrophilia in the lungs and in the exacerbation of Ag-induced pulmonary inflammation.
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THi cell differentiation is associated with epigenetic changes in the IL-17-IL-17F locus, which suggests novel mechanisms in T cell functional regulation.
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study found that THi cells upon stimulation produce not only IL-17 and IL-17F homodimers but also the IL-17A/F heterodimer; IL-17A/F cytokine represents another mechanism whereby T cells regulate inflammatory responses
