共查询到20条相似文献,搜索用时 15 毫秒
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EBV-induced gene 3 transcription is induced by TLR signaling in primary dendritic cells via NF-kappa B activation 总被引:7,自引:0,他引:7
Wirtz S Becker C Fantini MC Nieuwenhuis EE Tubbe I Galle PR Schild HJ Birkenbach M Blumberg RS Neurath MF 《Journal of immunology (Baltimore, Md. : 1950)》2005,174(5):2814-2824
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Multiple cis Regulatory Elements Control RANTES Promoter Activity in Alveolar Epithelial Cells Infected with Respiratory Syncytial Virus 下载免费PDF全文
Antonella Casola Roberto P. Garofalo Helene Haeberle Todd F. Elliott Rongtuan Lin Mohammad Jamaluddin Allan R. Brasier 《Journal of virology》2001,75(14):6428-6439
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Noulin N Quesniaux VF Schnyder-Candrian S Schnyder B Maillet I Robert T Vargaftig BB Ryffel B Couillin I 《Journal of immunology (Baltimore, Md. : 1950)》2005,175(10):6861-6869
Inhaled endotoxin induces an inflammatory response that contributes to the development and severity of asthma and other forms of airway disease. Here, we show that inhaled endotoxin-induced acute bronchoconstriction, TNF, IL-12p40, and KC production, protein leak, and neutrophil recruitment in the lung are abrogated in mice deficient for the adaptor molecule MyD88. Bronchoconstriction, inflammation, and protein leak are normal in Toll/IL-1R domain-containing adaptor inducing IFN-beta-deficient mice. MyD88 is involved in TLR, but also in IL-1R-associated kinase 1-mediated IL-1R and -18R signaling. We exclude a role for IL-1 and IL-18 pathways in this response, as IL-1R1 and caspase-1 (ICE)-deficient mice develop lung inflammation while TLR4-deficient mice are unresponsive to inhaled LPS. Significantly, using bone marrow chimera, we demonstrate that both hemopoietic and resident cells are necessary for a full MyD88-dependent response to inhaled endotoxin; bronchoconstriction depends on resident cells while cytokine secretion is mediated by hemopoietic cells. 相似文献
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Gu JQ Ikuyama S Wei P Fan B Oyama J Inoguchi T Nishimura J 《American journal of physiology. Endocrinology and metabolism》2008,295(6):E1390-E1400