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Interleukin-17 promotes angiogenesis and tumor growth.
A novel role for IL-17 is revealed as a CD4 T-cell-derived mediator of angiogenesis that stimulates vascular endothelial cell migration and cord formation and regulates production of a variety of proangiogenic factors.
IL-17 Enhances the Net Angiogenic Activity and In Vivo Growth of Human Non-Small Cell Lung Cancer in SCID Mice through Promoting CXCR-2-Dependent Angiogenesis1
It is demonstrated that IL-17 increases the net angiogenic activity and in vivo growth of NSCLC via promoting CXCR-2-dependent angiogenesis and suggest that targeting CX CR-2 signaling may be a novel promising strategy to treat patients with NSCLCs.
Bone Marrow-Derived Progenitor Cells Are Important for Lung Repair after Lipopolysaccharide-Induced Lung Injury 1
It is shown that LPS, a component of Gram-negative bacterial cell walls, in the lung airways, induces a rapid mobilization of BMPCs into the circulation in mice, and the suppression ofBMPCs by sublethal irradiation before intrapulmonary LPS leads to disruption of tissue structure and emphysema-like changes.
Microsatellite polymorphism in heme oxygenase-1 gene promoter is associated with susceptibility to oxidant-induced apoptosis in lymphoblastoid cell lines.
It is suggested that the polymorphism of the HO-1 gene is associated with the strength of antiapoptotic effects ofHO-1, resulting in an association with susceptibility to oxidative stress-mediated diseases.
Mechanisms of mucin production by rhinovirus infection in cultured human airway epithelial cells
Lipopolysaccharide (LPS)-binding protein stimulates CD14-dependent Toll-like receptor 4 internalization and LPS-induced TBK1–IKKϵ–IRF3 axis activation
It is shown that LBP-mediated LPS transfer to mCD14 is required for serum-dependent TLR4 internalization and activation of the TRIF pathway, which induces TLR adaptor molecule 1 (TRIF)-dependentactivation of the TBK1–IKKϵ–IRF3–IFN-β pathway.
Antitumor activity of type III interferon alone or in combination with type I interferon against human non‐small cell lung cancer
It is demonstrated that type III IFN can mediate direct antitumor activities via increased p21 expression and induction of apoptosis and cooperate with type I IFN to elicit more efficient direct antiproliferative activities, and the possibility that type II IFN might improve the efficacy and reduce the side‐effects of type IIFN cancer therapy is suggested.