标题:Tumor necrosis factor-α pathway plays a critical role in regulating interferon-γ induced protein-10 production in initial allogeneic human monocyte-endothelial cell interactions
作者:Fang,Y.S.;Zhu,L.M.;Sun,Z.G.;Yu,L.Z.;Xu,H.
通讯作者:Yu, LZ
作者机构:[Fang, Y.S] Department of Surgery, Jinan Central Hospital Affiliated to Shandong University, Jinan, China;[ Zhu, L.M] Department of Surgery, Jinan Cen 更多
会议名称:12th Congress of the Asian-Society-of-Transplantation (AST)
会议日期:SEP 25-28, 2011
来源:Transplantation Proceedings
出版年:2012
卷:44
期:4
页码:993-995
DOI:10.1016/j.transproceed.2012.03.051
摘要:T-cell infiltration of allografts is a major pathologic component defining acute rejection episodes (ARE). We have shown that monocytes interact with allogeneic endothelial cells (ECs) for costimulation to achieve T-cell allorecognition. However, the production of T-cell interferon-γ induced protein-10 (IP-10) and regulation of this chemokine during the initial monocyte-EC interaction are unclear. We hypothesized that the tumor necrosis factor (TNF)-α pathway plays a key role to regulate IP-10 production during the initial monocyte-EC interaction. Cytokine-activated ECs were analyzed for IP-10 production and adhesion molecule expression. Established, monocyte-EC cocultures were analyzed using real-time polymerase chain reaction and a chemokine assay for IP-10 and activation factors. Anti-TNF-α antibody was used to neutralize TNF-α release during monocyte-EC interactions. TNF-α-activated ECs upregulated CD62E and CD54 as determined by flow cytometry, releasing high levels of IP-10 and interleukin (IL)-6. Interferon-γ-stimulated ECs also produced high levels of IP-10 and IL-6. Monocyte-EC interactions demonstrated upregulation of gene transcripts for TNF-α, IL-6, and IP-10. The cytokine/chemokine assay detected high levels of TNF-α, IL-6, and IP-10 in coculture supernates in a time-dependent manner. Anti-TNF-α antibody dramatically reduced IP-10 production by monocyte-ECs interactions. However, anti-TNF-α antibody did not prevent the release of IL-6 by monocytes in EC cocultures. Our results showed that ECs activated by TNF-α are an important source of IP-10. The monocyte-EC interaction produces high levels of IP-10. The TNF-α pathway plays a key role to regulate IP-10 production during monocyte-EC interactions. We thus proposed that the initial monocyte-EC interaction with increased expression of IP-10 may play a critical role to initiate and augment T-cell-mediated ARE.
收录类别:CPCI-S;SCOPUS;SCIE
WOS核心被引频次:5
Scopus被引频次:6
资源类型:会议论文;期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84860765477&doi=10.1016%2fj.transproceed.2012.03.051&partnerID=40&md5=4f3e4658787441e2b3653150d324c052
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