共查询到20条相似文献,搜索用时 15 毫秒
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Nucelar NFκB was analyzed in murine Th2 cells after stimulation via the TCR pathway. Signals delivered through the TCR/CD3 complex induced active NFκB translocation to the nucleus of Th2 cells after a late phase (24 h) of the activation process, which is in contrast to the rapid appearance of nuclear NFκB (3 h) in Th1 cells after the same stimulation. The slow kinetic of NFκB nuclear uptake in Th2 cells was not accelerated by CD28 triggering or under stimulation with antigen plus antigen-presenting cells. Th1 and Th2 cells were also different in the composition of NFκB complexes induced. Whereas in Th1 cells TCR triggering induced the presence of nuclear p50.p65 heterodimers, in Th2 cells the complexes induced were shown to be composed of p65 plus another NFκB protein distinct from p50. The delayed NFκB induction in Th2 cells was dependent on protein synthesis and the significance of this is discussed. 相似文献
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Modified vaccinia Ankara (MVA) is an attenuated vaccinia virus, and is a promising vaccine vector for variola and monkeypox viruses, as well as for other pathogens. The MVA determinants important for vaccine efficacy and immunogenicity are poorly defined. MVA infection of fibroblast cells activates NF-κB, a characteristic not ascribed to wild-type vaccinia viruses. Thus, NF-κB activation, and the subsequent upregulation of host immune molecules, could be one of the determinants for MVA's immunogenicity. We report that ERK2 phosphorylation, an event preceding and required for NF-κB activation, occurred rapidly after virus infection. ERK2 and NF-κB remained inert when virus endocytosis was prevented, suggesting that virus–host cell interactions were insufficient for activating NF-κB. Inhibition of viral protein synthesis decreased NF-κB activation, and elimination of intermediate and late gene expression did not alter MVA-induced NF-κB activation. Thus, early gene expression activates NF-κB. 相似文献
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Gliosis is characterized by increased expression of glial fibrillary acidic protein (GFAP) and astroglial proliferation, although the mechanism underlying the process is still largely undefined. This study explores the role of the adenosine A2a receptor (A2aR) in gliosis after ischemia-like injury in a rat astrocyte cell line transfected with A2aR. A2aR transfection enhanced GFAP expression and cell proliferation. A2aR-selective antagonist Sch58261 decreased GFAP expression in a dose- and time-dependent manner with increased activation of Akt, and induced activation of NF-κB. An Akt inhibitor reversed the effect of Sch58261. These results suggest that the effect of A2aR on gliosis is related to the Akt/NF-κB signal pathway. 相似文献
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Although progesterone has been recognized as essential for the establishment and maintenance of pregnancy, this steroid hormone has been implicated to have a functional role in immune response, mainly at concentrations commensurate with pregnancy. However, the underlying mechanisms remain to be fully understood. Here we present the evidences that progesterone inhibited immune response to lipopolysaccharide (LPS) and CpG oligodeoxynucleotides (CpG ODNs) through modulating Toll-like receptor (TLR) signaling. Pretreatment with progesterone can significantly inhibit TLR4 and TLR9-triggered IL-6 and nitric oxide (NO) production in macrophages. Furthermore, we found that progesterone can significantly inhibit LPS-induced nitric oxide synthesis (iNOS), TLR4 expression and nuclear factor-κB (NF-κB) activation. Consistently, as a negative feedback inhibitor, the expression of suppressor of cytokine signaling (SOCS1) protein was up-regulated by progesterone in LPS-stimulated macrophages. These results support the concept that progesterone might inhibit innate immune response by suppressing NF-κB activation and enhancement of SOCS1 expression, providing a possible mechanistic explanation for the function of progesterone in regulating innate immune responses. 相似文献
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S. Tanaka S. Nishiumi M. Nishida Y. Mizushina K. Kobayashi A. Masuda T. Fujita Y. Morita S. Mizuno H. Kutsumi T. Azuma M. Yoshida 《Clinical and experimental immunology》2010,160(2):283-292
Vitamin K is a family of fat‐soluble compounds including phylloquinone (vitamin K1), menaquinone (vitamin K2) and menadione (vitamin K3). Recently, it was reported that vitamin K, especially vitamins K1 and K2, exerts a variety of biological effects, and these compounds are expected to be candidates for therapeutic agents against various diseases. In this study, we investigated the anti‐inflammatory effects of vitamin K3 in in vitro cultured cell experiments and in vivo animal experiments. In human embryonic kidney (HEK)293 cells, vitamin K3 inhibited the tumour necrosis factor (TNF)‐α‐evoked translocation of nuclear factor (NF)‐κB into the nucleus, although vitamins K1 and K2 did not. Vitamin K3 also suppressed the lipopolysaccharide (LPS)‐induced nuclear translocation of NF‐κB and production of TNF‐α in mouse macrophage RAW264·7 cells. Moreover, the addition of vitamin K3 before and after LPS administration attenuated the severity of lung injury in an animal model of acute lung injury/acute respiratory distress syndrome (ARDS), which occurs in the setting of acute severe illness complicated by systemic inflammation. In the ARDS model, vitamin K3 also suppressed the LPS‐induced increase in the serum TNF‐α level and inhibited the LPS‐evoked nuclear translocation of NF‐κB in lung tissue. Despite marked efforts, little therapeutic progress has been made, and the mortality rate of ARDS remains high. Vitamin K3 may be an effective therapeutic strategy against acute lung injury including ARDS. 相似文献
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