TNFSF14 coordinately enhances CXCL10 and CXCL11 productions from IFN-γ-stimulated human gingival fibroblasts
TNFSF14 coordinately enhances CXCL10 and CXCL11 productions from IFN-γ-stimulated human gingival fibroblasts
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DOI：
10.1016/j.molimm.2009.10.018
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发表时间：
2010-01-01
影响因子：
3.6
通讯作者：
Matsuo, Takashi
中科院分区：
文献类型：
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作者：
Hosokawa, Yoshitaka;Hosokawa, Ikuko;Matsuo, Takashi
TNFSF 14参与了一些炎性疾病如关节炎的发病机制。CXCL 10和CXCL 11募集Th 1细胞，这些趋化因子的产生与关节炎和牙周病等炎症性疾病的加重有关。我们研究了TNFSF 14对IFN-γ诱导的人牙龈成纤维细胞（HGF）中CXCL 10和CXCL 11产生的体外作用。HGF组成型表达TNFSF 14受体、LT β R和HVEM。TNFSF 14增强IFN-γ诱导的HGFs分泌CXCL 10和CXCL 11。IFN-γ处理增加HGF上的HVEM表达。与单独的TNFSF 14或IFN-γ相比，TNFSF 14与IFN-γ组合导致p38 MAPK、ERK和I κ B-α的活化增加。此外，p38 MAPK、ERK和NF-κ B的抑制剂消除了TNF-α 14与IFN-γ刺激的HGF产生的CXCL 10和CXCL 11。TNFSF 14的这些作用可能促进Th 1细胞浸润到炎性疾病的病变中。TNFSF 14可能在某些炎症性疾病中作为促炎细胞因子发挥作用，因此是一个候选的治疗靶点。(C)2010爱思唯尔有限公司版权所有。
TNFSF14 is involved in the pathogenesis of some inflammatory diseases such as arthritis. CXCL10 and CXCL11 recruit Th1 cells, and the productions of these chemokines are related to the exacerbation of some inflammatory diseases including arthritis and periodontal disease. We examined in vitro effects of TNFSF14 on IFN-gamma-induced CXCL10 and CXCL11 production in human gingival fibroblasts (HGFs). HGFs constitutively expressed TNFSF14 receptors, LT beta R and HVEM. TNFSF14 enhanced IFN-gamma-induced secretion of CXCL10 and CXCL11 from HGFs. IFN-gamma treatment increased HVEM expression on HGFs. TNFSF14 in combination with IFN-gamma resulted in increased activation of p38 MAPK, ERK and I kappa B-alpha compared with TNFSF14 or IFN-gamma alone. Moreover, inhibitors of p38 MAPK, ERK and NF-kappa B abolished the CXCL10 and CXCL11 productions from TNFSF14 with IFN-gamma-stimulated HGFs. These effects of TNFSF14 may promote the infiltration of Th1 cells into lesions with inflammatory diseases. TNFSF14 might act as a proinflammatory cytokine in some inflammatory diseases thus is a candidate therapeutic target. (C) 2010 Elsevier Ltd. All rights reserved.