IL-17A/F Modulates Fibrocyte Functions in Cooperation with CD40-Mediated Signaling
作者： Hisako Hayashi , Akiko Kawakita , Shintaro Okazaki , Motoko Yasutomi , Hiroki Murai
DOI: 10.1007/S10753-013-9609-Z
关键词:
摘要: T helper 17 (Th17) cells that produce interleukin (IL)-17A and IL-17F have been found to participate in the development of bronchial asthma bleomycin-induced pulmonary fibrosis. However, whether they play a causative role airway remodeling observed these respiratory diseases remains unclear. Because fibrocytes are involved tissue repair fibrosis presumably precursors lung fibroblasts myofibroblasts, we examined effects IL-17A/F on fibrocyte functions. Both IL-17A enhanced fibrocytes' α-smooth muscle actin expression. Priming with their CD40-mediated IL-6 production, whereas IL-17F-priming increased mRNA expression collagen I, vascular endothelial growth factor, angiogenin. CD4(+) co-cultured produced IL-17A, which was inhibited by blocking CD40 ligand interactions. These findings suggest cooperative interactions between Th17 an important via CD40- IL-17A/F-mediated signaling for proangiogenic factor may lead extracellular matrix deposition neovascularization seen remodeling.
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