Journal
FRONTIERS IN PHARMACOLOGY
Volume 5, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2014.00002
Keywords
Idiopathic pulmonary fibrosis (IPF); lung fibroblasts; myofibroblasts; Toll Like Receptor 9 (TLR9); C-C Chemokine receptor type 7 (CCR7); interleukin 6 (IL6); glycoprotein 130 (gp130); C-C motif chemokine ligand 21 (CCL21)
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Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease characterized by the persistence of activated myofibroblasts resulting in excessive deposition of extracellular matrix proteins and profound tissue remodeling. Myofibroblasts have been shown to arise from interstitial fibroblasts, epithelial to mesenchymal transition of type II alveolar epithelial cells, and the differentiation of recruited fibrocytes. There are many mechanisms that are utilized by these cells for survival, proliferation, and persistent activation including up-regulation of cytokines [i.e., Interleukin 6 (IL6) and C-C motif chemokine ligand 21 (CCL21)1, cytokine receptors [i.e., Interleukin 6 Receptor 1 (IL-6R1), Glycoprotein 130 (gp130) and C-C Chemokine Receptor type 7 (CCR7)], and innate pattern recognition receptors [(PRRs; i.e., Toll Like Receptor 9 (TLR9)]. In this review, we will discuss the role of the cytokines IL-6 and CCL21, their receptors and the PRR, TLR9, in fibroblast recruitment, activation, survival, and differentiation into myofibroblasts in IPF.
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