PATHOLOGY

Detailed explanation-1: -The canonical IL-17 signaling pathway initiates signaling through Act1-induced K63-linked ubiquitylation of TRAF6, thereby activating the mitogen-activated protein kinase (MAPK), CCAAT-enhancer-binding protein (C/EBP), and nuclear factor B (NF-B) pathways.

Detailed explanation-2: -IL-17 promotes granulopoiesis and mobilization of mature neutrophils from the bone marrow by acting through upregulation of granulocyte colony-stimulating factor. Upon release from the bone marrow, circulating neutrophils can normally extravasate into infected or inflamed tissues.

Detailed explanation-3: -The IL-17 functions in this setting by inducing genes encoding Regulator of G-protein signalling 13 and 16 (Rgs13 and Rgs16), which inhibit G-coupled protein receptors such as CXCR4.

Detailed explanation-4: -The treatment of fibroblasts with IL-17A results in the upregulation of several cytokines, including chemokine (C–X–C motif) ligand 1 (CXCL1), chemokine (C–C motif) ligand 2 (CCL2), CCL7, CCL20 and matrix metalloproteinase 3 and 13. Similar results were obtained using a lung epithelial cell line.