医学写作精挑句子.doc

This study used the well-characterized epithelial HeLa cell line as anexperimental model system to investigate the first steps of transcription factor binding leading to induction of IL-6 expression by IR. After transient transfection by IR.Thus, to delineate the role of the proximal elements a mutation was introduced into pIL6-1180 which destroyed its ability to interact with AP-1 transcription factors. A multifactorial stress response was found involving three transcription factor recognition elements of the IL-6 promoter, NF-kB, AP-1 and MREWe report here that Fk and IL-1 synergistically enhance IL-6 mRNA expression in FRTL-5 thyroid cells by mechanisms involving the cAMP/PKA pathway, and both stabilization of the IL-6 mRNA and activation of the IL-6 promoter. Point mutations or deletions of the main transcription factor binding sites in the IL-6 promoter indicated that the synergistic effect was mainly mediated by the AP-1 site, and that the CRE site contributed to this effect.These ndings contribute to elucidating the synergistic mechanisms that.，, and suggest that.We will then examine the role of NFkB in regulating cytokine production, explore the intricate system of positive and negative feedback loops that control NFkB activation, and evaluate current information about the significance of NFkB in the pathobiology of diseasequiescent cellsFollowing a stimulus, cytokines are produced in a characteristic pattern that is dependent on the stimulus as well as the cell or tissue type.Of particular importance is thatBy means of South-Western blottingFlagellin induces IL-6 production in concentration- andtime-dependent fashionToday, various links have been established between chronic inflammation and cancer, converging on the transcription factor NF-BIn this respect, cancer chemopreventive natural compounds, such as Withaferin A, genistein, curcumin, and green tea polyphenols, which interfere with multiple oncogenic pathways converging on the transcription factors NF-B and AP-1 ,may soon join the arsenal of epigenetic drugsTherefore it is imperative to clarify the regulatory mechanism of the IL-6 gene expression for understanding the deregulation of the IL-6 gene expression and finally the pathogenesis of IL-6-associated disorders.Synthetic oligonucleotides (ODN) expressing CpG motifs mimic the ability of bacterial DNA to trigger the innate immune system via TLR9. Plasmacytoid dendritic cells (pDCs) make a critical contribution to the ensuing immune response.up-modulators up-modulationLater Naitoh et al. (7) showed that IL-6 administered i.v. stimulated theincrease of ACTH secretion in conscious, freely moving rats.Interleukin-6 (IL-6) is a pleiotropic cytokine that is implicated in endocrine and metabolic actions, as well as in immune regulation and aging。Previously we have demonstrated that the IL-6 promoter activity results from a concerted cooperation between NF-kB, AP-1, CREB, and C/EBP transcription factorsStudies aimed at elucidating their mechanism of action could therefore contribute to the design of antiinflammatory compounds devoid of side effects.Hence, numerous local and systemic regulatory pathways have evolved to curb inflammationActivation of MC is thought to be intimately associated with the pathogenesis of glomerulonephritis, ultimately leading to irreversible functional damage of the filtering apparatusInflammation-repressing patternBy association withThe cells of the immune system are broadly divided into those that belong to the innate arm of immunity and those that belong to the adaptive immune systemOn the adaptive side of immunity,CBF1 has also been reported to function as a transcription repressor per se by competing with activators of the Rel family at overlapping binding sitesWe compare the characteristics of strokeincluding the sites of immune action, the timing dynamics of inflammation, and the spectrum of immune responsewith those of multiple sclerosis (MS), which is a classic inflammatory and autoimmune disorder of the CNSour studies suggest that CTLA-4 ligation of CD80 is required for TGF- to induce FoxP3 and generate suppressor T cells.This agent, however,will also block CTLA-4 ligation to B7.Once activated, they can themselves produce immunoregulatory cytokines and regulate the development of the ensuing immune response and tissue inflammation,as well as kill target cells.with certain stimulations such as MPTP intoxication, the AQP4 KO mice showed extraordinarily more robust inflammatory responses than WT miceTo determine the potential of Tregs to inhibit T cell proliferation, naiveCD4CD25T cells were stimulated with anti-CD3 and cultured with graded amounts of Tregs, which inhibited anti-CD3-induced mitogenesis in a dose-dependent manner, providing maximal suppression (62%) at a 1:1 Treg:Teff ratio.Recent studies have demonstrated that plasticity of naturally occurring nTregs may account for their inability to control chronic inflammation in established autoimmune diseasesvitamin A metabolite RA as a key regulator of TGF-beta dependent immune responses, capable of inhibiting the IL-6 driven induction of proinflammatory TH17 cells and promoting antiinflammatory Treg cell differentiation.These observations indicate that the priming of T cells by DCs in the presence of TGF-b might lead to opposing immune consequencesinflammatory cytokines took the responsibility for the upregulation of AQP4 by activating the p38 signaling pathway.Now, a new homeostatic role is emerging for RA as a regulator of biological rhythms within the CNSthe autophagy-related gene 5 (ATG5) has emerged as a spotlight in a multitude of immune functionsAs a lineage fate determinant factor of nTregs, Foxp3 is essential and sufficient for its development and immunosuppressive activityWe identified a heretofore-unappreciated role for the RAR in driving T cell immunity.RA, in particular, has been shown previously to induce strong effects on a variety of immune cell populations in vitro and in vitamin A-replete settings in vivoBefore transfer and weekly thereafter, blood was collected,ATRA also significantly decreased the number of Foxp3- cells in the CD4- cells,indicating that ATRA selectively promotes CD4+Foxp3+ cell conversion.After the CD4+Foxp3+ cells had been induced, the addition of ATRA maintained but did not expand the number of Foxp3+ cells.It is likely that ATRA mostly affects the differentiation rather than the expansion of Foxp3+ cellsSuch inhibition was paired with a decreased (IFN)gamma and (TNF)alpha production and was partially reversed by interleukin-2 (IL-2).MSCs have been considered to be an ideal cellular source for GVHD treatment due to their unique properties, including tissue repair and major histocompatibility complex (MHC)-unmatched immunosuppression.Therapeutic manipulation of purified Foxp3+ cells provides a logical rationale for a promising alternative approach to treat many autoimmune diseases, yet isolating and enriching viable purified Foxp3-positive cells remains a major challengeOur results showed that coculture with iTreg cells led to a cell number dependent inhibition of PMACI-stimulated TNF-a and IL-6 release by BMMCs, with a maximum inhibitory effect at a 2:1 (BMMCs/iTreg cells) ratioTo investigate the role of iTregs in this process and compare their functional characteristics with nTregs, we injected 3106 iTregs or nTregs at the time of CIA challengeAs previously described, skewing of responses towards Th17 and away from BMSCs or Treg cells may be responsible for the development and/or progression of ASActive vitamin D alters the phenotype and functionality of DCs, locking them in a nonmature state, with features of tolerogenic DCsA recent s