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Gene Review

IL6  -  interleukin 6

Homo sapiens

Synonyms: B-cell stimulatory factor 2, BSF-2, BSF2, CDF, CTL differentiation factor, ...
 
 
 
Georg Haerter, Wendy B. London,  Lampe,  Wichter,  Cornér,  Koelbl,  Fisher,  Bernig,  Heinze, Thomas Berg,  Thorp,  Santini,  Patel, Juliane Halangk, Thomas Lutz, Joanne P. Lagmay,  Hamsten,  Kannisto,  Deng,  Ringheim, Hans Dieter Nischalke,  Eschert,  Kolak, Hans Dieter Nischalke,  Hanisch, Heidi V. Russell,  Deng,  Koehl,  Reinthaller, David S. Siscovick, Martin Vogel,  Korsheninnikova, Baumgarten Axel,  Chanock,  Böhm, Mark Ranalli, Jacob Nattermann,  Zhu, Amanda Termuhlen,  Hefler,  Reinhardt,  Tong-Cacsire, Brigitte Banas, Jacob Nattermann,  Liljeroth, Georg Feldmann,  Nyman,  Ferrannini,  Tarkowski,  Shi, Susan M. Burlingame, Amy Axel, Bonaventura Clotet, Bernhard Bienek,  Klingebiel, Tilman Sauerbruch,  Tarkowski, Russell P. Tracy, Tilman Sauerbruch,  Blennow,  Wallin, Thomas Berg,  Gong,  Solini, Catherine M. Cahill,  Lantzsch,  Engel, Juergen K. Rockstroh, Michael Rausch,  Leodolter,  Lehrnbecher,  Flesch, Wolfgang H. Caselmann, Jack T. Rogers, Mark Danta, Christina Tural,  Burgher,  Chanock,  Grimm, Wolff Schmiegel,  Shah, Jed G. Nuchtern, Brett Hall,  Guo, Nicholas Sullivan,  Makkonen,  Olshan,  Szczepanik,  Behl,  Erichsen, Christoph Mayr,  Erren,  Zeillinger, Christian Teschendorf,  Schwabe,  Westerbacka, Ulrich Spengler,  Tempfer, Knud Schewe, Patrick McGrady,  Creutzig,  Plenz, Agathe Iwan, Jason Canner,  Nannipieri, Gerd Klausen,  Chao, Kenneth J. Mukamal,  Scheld, Thomas G. Gross, Ulrich Spengler, Raffaele Bruno, Ulrich Dührsen, Rachel A. Egler,  Sehgal,  Minthon, Nancy S. Jenny,  Petko,  Yki-Järvinen, Bethany Mundy,  Savitz,  Kumar, Frank Grünhage,  
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Disease relevance of IL6

 

Psychiatry related information on IL6

  • It appears that BSF2/IL-6 plays an essential role in the host defense mechanisms against infections, inflammation, and injury [8].
  • The capacity for sIL-6R to enhance IL-6 function and broaden the IL-6 target cell population in the brain has implications for the regulation of beta-APP expression in disease states such as Alzheimer's disease where elevations in brain IL-6 levels have been reported [9].
  • Depressive symptoms following IFNalpha treatment may be secondary to cytokine induction, including that of IL-6 [10].
  • CONCLUSIONS: The results suggest that PTSD is associated with increased IL-6 signaling [11].
  • Our results, which show for the first time strikingly increased CSF levels of TNF-alpha but not of TNF-beta, IL-1beta or IL-6 in AD and VAD, may form a conceptual framework for further studies of neuroprotective mechanisms in dementias [12].
  • Among older adults free of clinical cardiovascular disease, specific IL-6 promoter and apo E alleles appeared to confer positive associations of alcohol consumption with IL-6 concentrations [13].
 

High impact information on IL6

  • A signaling adapter function for alpha6beta4 integrin in the control of HGF-dependent invasive growth [14].
  • Like HGF, InlB binds to the extracellular domain of Met and induces "scattering" of epithelial cells [15].
  • Treatment of mammalian cells with InlB protein or infection with L. monocytogenes induces rapid tyrosine phosphorylation of Met, a receptor tyrosine kinase (RTK) for which the only known ligand is Hepatocyte Growth Factor (HGF) [15].
  • In contrast, we observed that p91 is not tyrosine phosphorylated in response to IL-6 [16].
  • Here, we report the existence in the hepatocyte growth factor/scatter factor (HGF/SF) receptor of a multifunctional docking site made of the tandemly arranged degenerate sequence YVH/NV [17].
 

Chemical compound and disease context of IL6

 

Biological context of IL6

 

Anatomical context of IL6

  • This study demonstrates that LMP1 expression in carcinoma cell lines and SV40-transformed keratinocytes results in induction of the pleiotropic cytokine interleukin 6 (IL6), an effect which is also observed upon CD40 ligation [25].
  • OBJECTIVES: To assess the potential of the donor heart to respond to interleukin-6 (IL6), the present study investigated the expression of IL6 receptor components in the myocardium of donor hearts before transplantation [26].
  • While IL6 was mainly expressed by myocytes, both receptor components were preferentially found mainly on interstitial cells [26].
  • Right ventricles of failing hearts showed IL6, IL6R and gp130 mRNA levels comparable with those found in donor hearts [26].
  • On the other hand, it appears that IL-6R expression by primary hepatocytes is sufficient and that circulating sIL-6R is unlikely to play a significant role in the modulation of IL6 effects [27].
 

Associations of IL6 with chemical compounds

  • CONCLUSIONS/INTERPRETATION: Homocysteine upregulates the MMP-TIMP pathway and IL6 release, the effect being stronger in the presence of high glucose [28].
  • METHODS: We investigated the relationship of polymorphisms in 6 cytokine genes associated with inflammation-interleukin (IL)1alpha, IL1beta, IL2, IL6, tumor necrosis factor (TNF), and lymphotoxin alpha (LTA)-with spontaneous preterm and SGA birth in a nested case-control study drawn from a prospective pregnancy cohort [29].
  • The reappearance of IL6-binding sites at the cell surface required greater than 8 h and was sensitive to cycloheximide, suggesting that gp80 is not recycled after internalization [30].
  • Thus, a general first step in IL-6-related cytokine signaling may be the dimerization of signal-transducing molecules and activation of associated tyrosine kinases [31].
  • The median levels of PCA, TNF-alpha, and IL-6 were 5, 0, and 4%, respectively, of the monocyte activities induced by normal plasma boosted with purified N. meningitidis (Nm)-LPS (2,500 pg/ml; net LPS-boosted capacity, 100%) [18].
  • These data suggest that the stimulatory effects of insulin on IL-6 release involve several interrelated components: transcription, intracellular releasable pool, and secretion, which are differentially regulated and, thus, determine the size of the releasable pool of IL-6 [32].
  • Further investigations into the signaling mechanisms regulating IL-6 production led to the discovery that the Tec kinase bone marrow tyrosine kinase gene in chromosome X (Bmx) regulates Toll-like receptor-induced IL-6 production [33].
  • Without exogenous IL-6/sIL-6R, injury plus TNFalpha exposure up-regulated chondrocyte production of IL-6, but incubation with the IL-6-blocking Fab significantly reduced proteoglycan degradation [34].
  • Bicalutamide showed an inhibitory effect on IL-6-regulated growth in vivo [35].
 

Physical interactions of IL6

  • The TNF-alpha mediated transcriptional activation of a chloramphenicol acetyltransferase (CAT) plasmid containing three copies of the -72 kappa B binding site from the IL-6 promoter was abrogated by PDTC [36].
  • We studied the capacity of these mutants to form an IL-6/IL-6R complex and their ability to transduce the signal [37].
  • A corresponding gp130-binding site on IL-6 was exchanged with this epitope [38].
  • Recently, we showed that the magnitude of Stat3 binding to three IL-6 motifs on the human gammaFBG promoter correlates negatively with their functional activity in hepatocytes, although these cis-elements are critical for promoter activity [39].
  • Moreover, titration of sgp130 with OM inhibits the formation of a ternary complex comprising IL-6, sIL-6R alpha, and sgp130 [40].
 

Enzymatic interactions of IL6

  • Upon activation of signaling by IL-6 or orthovanadate the respective Tyr-phosphorylated STAT species were now also observed in the membrane raft fraction but in a form deficient in DNA binding [41].
  • RESULTS: We report that NSCLC cells overexpressing COX-2 (COX-2-S) have increased IL-6 and phosphorylated STAT3 expression compared with control cells [42].
  • Also p27 protein accumulated which coincided with the disappearance of hyperphosphorylated retinoblastoma protein in three human melanoma cell lines sensitive to IL-6-type cytokines [43].
  • Western blot analysis demonstrated that IL-6 indeed increased the activation of phosphorylated MEK and p38 MAPK in GH3 cells [44].
  • METHODS: The effect of IL-6 on apoptosis induced by androgen deprivation in LNCaP cells was examined by cell death ELISA and Western blot using cleaved poly (ADP-ribose) polymerase (PARP) and caspase-9, as well as Bcl-xL and phosphorylated Bad [45].
 

Co-localisations of IL6

  • Furthermore, FKHR and STAT3 were shown to coimmunoprecipitate and to colocalize in the nuclear regions of IL-6-treated HepG2 cells [46].
 

Regulatory relationships of IL6

  • IL-6-induced homodimerization of gp130 and associated activation of a tyrosine kinase [31].
  • However, significantly more IL-7 than IL-1 beta was required to induce detectable levels of IL-6 [47].
  • In contrast to the low concentrations of IL-7 required to stimulate T cell growth and differentiation (as low as 0.1 ng/ml), relatively high concentrations of IL-7 were necessary to induce IL-6 secretion by monocytes (at least 10 ng/ml) [47].
  • IL-6 induced STAT3 phosphorylation and activation in HOSE cells; STAT3 was constitutively activated in OVCA cells [48].
  • The IL-8-induced inhibition was counteracted by IL-6 and tumor necrosis factor-alpha (TNF-alpha) and was blocked by anti-IL-8 monoclonal antibody (MoAb) [49].
  • Vice versa, inactivation of IL-6 autocrine loop had no influence on apoptosis levels in the absence of Mcl-1, thus suggesting this molecule as a mediator of the survival action of IL-6 [50].
  • IL-6 treatment triggered Notch-3-dependent upregulation of the Notch ligand Jagged-1 and promotion of MS and MCF-7-derived spheroid growth [51].
 

Other interactions of IL6

  • RESULTS--Mean serum IL-6 levels, but not IL-1 beta or tumor necrosis factor-alpha levels, correlated with organ failure (r = 0.79, P < .001) [52].
  • Subsequently, the plasma is removed, medium added, and procoagulant activity (PCA) and secretion of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) measured after 18-h incubation [18].
  • Moreover, addition of IL-5 or IL-6 did not reverse IL-8-induced inhibition of IgE production [53].
  • These results indicate that histamine enhanced IgE and IgG4 production by increasing endogenous IL-6 and IL-10 production via H1 and H3 receptors, respectively [54].
  • Addition of anti-mu potentiated the effect of IL-4 on IL-6 production [55].
  • IL-6 induction was mediated via Toll-like receptor 2 (TLR2) and lead to increased B-cell proliferation in vitro [56].
  • Response rates to HCV-specific treatment are higher in HCV/HIV-positive patients carrying the IL-6 HP genotype, which might be because of IL-6 mediated STAT3 activation [57].
  • Only partial inhibition by dominant-negative AKT and no inhibitory effect of IKKalphaT23A was observed on an IL-6 promoter-specific NFkappaB site in contrast to significant inhibitory effects on the AP-1 site [58].
 

Analytical, diagnostic and therapeutic context of IL6

References

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