ライフサイエンスコーパス: IL-6R

1 IL-6R mRNA and protein were not detected in controls, bu

2 IL-6R protein expression was observed in bronchoalveolar

3 IL-6R signaling activates the transcription factor STAT1

4 This finding reveals a GATA3/miR-125a-5p/IL-6R and STAT3/FOXP3 regulatory pathway, which determin

5 Significant upregulation in IL-6, IL-6R, and gp130 occurred only at 24 hours of sustained

6 roles for CLCF1-CNTFR and interleukin (IL)-6-IL-6R signaling in promoting growth of NSCLCs.

7 ignaling, it acts as a spacer to ensure IL-6.IL-6R.gp130 signal complex formation.

8 This suggests that anti-IL-6/IL-6R blockade could be effective in modifying T- and B-

9 L-6 trans-signaling through the soluble IL-6/IL-6R complex is involved in this process.

10 presenting cells synthesize and express IL-6/IL-6R complexes, which are transported through the cell

11 Here, we explore the biology of IL-6/IL-6R interactions and the evidence for an important rol

12 autiously optimistic that targeting the IL-6/IL-6R pathway could offer a novel alternative for diffic

13 IL-6/IL-6R signaling pathway, in particular, has been propose

14 o determine effectiveness of inhibiting IL-6/IL-6R to ameliorate chronic allograft rejection and coro

15 s any cell, and the recently discovered IL-6/IL-6R transpresentation in which antigen-presenting cell

16 amples, some Th2 genes (IL-3, IL-5, and IL-6/IL-6R) were found to be up-regulated as well.

17 t]) and tocilizumab or siltuximab (anti-IL-6/IL-6R).

18 The mRNAs for LIF/LIFR, IL-6/IL-6R, and their common signal-transduction molecule, gp

19 t MAOA is down-regulated as a result of IL-6/IL-6R/STAT3 signalling and epigenetic mechanisms, effect

20 suppresses tumor progression by inhibiting a IL-6R/STAT3/miR-34a feedback loop.

21 that endothelial cell-derived IL-6 activates IL-6R (IL-6 Receptor) and signal transducer and activato

22 An active IL-6R/STAT3/miR-34a loop was necessary for EMT, invasion

23 actor receptor (EGFR) and the high-affinity, IL-6R/gp130-derived pY-peptide, GpYLPQTV-NH(2).

24 mbrane-bound or soluble IL-6 receptor alpha (IL-6R, sIL-6R), which is referred to as classic and tran

25 Importantly, although IL-6R deficient mice were strongly affected by PHX, surv

26 ponsiveness to IL-6 via the activation of an IL-6R sheddase, resulting in an immediate production of

27 Therefore, we generated and analyzed IL-6R stalk region deletion variants for cleavability an

28 In contrast, IL-2ralpha and IL-6R associations were found to be T cell specific.

29 well as associations between IL-2ralpha and IL-6R with several other IMDs.

30 -regulation of expression of LIFR, IL-6, and IL-6R in ensheathing cells by 3 days post-OBX.

31 CB1R and IL-6R co-stimulation enhanced the differentiation of rat

32 itself has no effect, we found that CB1R and IL-6R stimulation together induced synergistic neurite o

33 s and myeloid suppressors with TMZ-CD40L and IL-6R blockade.

34 will allow discriminating between CNTFR- and IL-6R-mediated effects in vivo.

35 IL-6 responses by CD34(+) cell cultures and IL-6R neutralization inhibited myeloid differentiation a

36 te direct binding of vIL-6 to both gp130 and IL-6R and vIL-6-induced gp130-IL-6R complex formation, a

37 , investigating the utilization of gp130 and IL-6R by vIL-6, and undertaking mutational analyses of v

38 mutational analyses of regions of gp130 and IL-6R potentially involved in interactions with ligand o

39 n, tumor cell-derived IL-6 induced gp130 and IL-6R-dependent activation of STAT3, leading to reduced

40 be involved directly in binding to gp130 and IL-6R.

41 residues important for IL-6R-independent and IL-6R-dependent signaling through native gp130 and gp130

42 that are important for IL-6R-independent and IL-6R-mediated functional complex formation between vIL-

43 B expression but restored IL-2 secretion and IL-6R and TGFbRII expression and signaling, as illustrat

44 Anti-IL-6R, selective blockade of sIL-6R, or gammadelta T-cel

45 mphasize caution for therapeutic use of anti-IL-6R antibody.

46 xpected, based on reports of the use of anti-IL-6R in inflammatory bowel disease, dnTGFbetaRII IL-6(-

47 Administration of anti-IL-6 or anti-IL-6R to wild-type recipients prior to transfer of CD8(-

48 Initial data from our group suggest anti-IL-6R therapy is of value in desensitization and prevent

49 Tocilizumab (anti-IL-6R) is approved by the Food and Drug Administration f

50 All patients were treated with anti-IL-6R antibody and/or IVIG, which led to rapid disease r

51 signaling; in this model treatment with anti-IL-6R did not suppress airway inflammation.

52 the best candidates for treatment with anti-IL-6R if they have accompanying autoimmune liver disease

53 Preemptive treatment of mice with anti-IL-6R or anti-IL-6 worsened NTN, whereas selective block

54 vels of IL-6 signaling intermediates such as IL-6R and signal transducer and activator of transcripti

55 lone did not induce T cell survival, because IL-6R expression on T cells in AqH was too low to facili

56 se results document that vIL-6 does not bind IL-6R and suggest that conformational change may be crit

57 3, an oncolytic adenovirus designed to block IL-6R signaling and to provide myeloid cell activation v

58 e ADAM17 cleavage site substantially blocked IL-6R proteolysis by ADAM17 but only slightly affected p

59 various diseases, the origin of blood-borne IL-6R is still poorly understood.

60 ved primary human osteoblasts expressed both IL-6R and gp130 as determined by flow cytometry and immu

61 acetate induced a dramatic increase of both IL-6R shedding (i.e. the production of sIL-6R) and IL-6

62 lassically orchestrated via a membrane-bound IL-6R (CD126) alpha subunit (classical IL-6R signaling)

63 oteases, IL-6 in complex with membrane-bound IL-6R and gp130 activates classic signaling.

64 IL-6R mAb that binds to both membrane-bound IL-6R and soluble IL-6R with the unique property of spec

65 by genetic conversion of all membrane-bound IL-6R into sIL-6R proteins phenocopying hyperactivation

66 ently, IL-6 signaling through membrane-bound IL-6R seems to be limited to naive or central memory T c

67 However, the membrane-bound IL-6R was nonfunctional, as significant tyrosine phospho

68 s mediated by shedding of the membrane-bound IL-6R, and this process correlates with the expression o

69 or 201-206 promoted a loss of membrane-bound IL-6R, suggesting release by proteolytic shedding.

70 IL-6 can signal through the membrane-bound IL-6R, which is expressed only on hepatocytes and certai

71 with similar affinity as the membrane-bound IL-6R.

72 ells' in vivo angiogenic capacity induced by IL-6R, which simultaneously activates Jak/STAT and PI3K/

73 s, as well as increased expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defectiv

74 selective IL-6 receptor deletion in T cells (IL-6R-cKO), we demonstrated that T cell-specific IL-6R s

75 Although circulating IL-6R levels are altered in various diseases, the origin

76 bound IL-6R (CD126) alpha subunit (classical IL-6R signaling) or through a soluble form of this cogna

77 Therefore, we concluded that classical IL-6R signaling in naive or central memory CD4(+) T cell

78 ng, the identity of the protease(s) cleaving IL-6R in more physiological settings, or even in vivo, r

79 Cognate IL-6R was detected in aortic smooth muscle, but its leve

80 iption-3 activation are mediated via cognate IL-6R.

81 atRA decreased IL-6R expression and signaling by nTregs.

82 , whereas constitutive release of endogenous IL-6R is largely mediated by ADAM10.

83 eficient mice we established that endogenous IL-6R of both human and murine origin is shed by ADAM17

84 chemistry was used to qualitatively evaluate IL-6R protein expression in bronchoalveolar lavage cells

85 ion experiments in Hep3B cells (that express IL-6R and gp130) showed that most were able to function

86 subset of naive CD8(+) T cells that express IL-6R into a unique population of effector CD8(+) T cell

87 Mice with a mutation in T cell-expressed IL-6R were unable to expand Tfh populations after HDM se

88 r this unused vIL-6 surface is available for IL-6R binding.

89 Tissues were immunostained for IL-6R, gp130, CD15(+) (polymorphonuclear), and CD3(+) (T

90 variants to identify residues important for IL-6R-independent and IL-6R-dependent signaling through

91 ied residues in vIL-6 that are important for IL-6R-independent and IL-6R-mediated functional complex

92 e antibody to IL-6, as was also observed for IL-6R mutants of Phe(279) In the second antibody, the si

93 Dual immunohistochemical staining for IL-6R and CD31 revealed IL-6R expression on human endoth

94 pressing proteolytic cleavage of sIL-6R from IL-6R and downregulation of the SOCS3 autoinhibitory pat

95 In contrast, Tfh cells from IL-6R-cKO-infected mice exhibited reduced ICOS expressio

96 Further, IL-6R blockade prevented upregulation of programed death

97 both gp130 and IL-6R and vIL-6-induced gp130-IL-6R complex formation, and we have extended our functi

98 s unique, involving classic signaling (IL-6->IL-6R) cell membrane receptors, transsignaling (IL-6->so

99 naling by endogenous IL-6 proteins; however, IL-6R can enhance vIL-6 activity and can enable signalin

100 agonistic cytokine via the murine and human IL-6R, indicating that p28 exhibits no species specifici

101 ed NI-1201, a mAb that targets, in the human IL-6R sequence, the epitope recognized by 25F10 for mice

102 from variation in IL-6 and more importantly IL-6R.

103 the metalloproteinases ADAM10 and ADAM17 in IL-6R shedding, the identity of the protease(s) cleaving

104 cells in vitro leads to a downregulation in IL-6R expression.

105 ly conserved, alpha-helical, and involved in IL-6R binding.

106 gest haplotype associations were observed in IL-6R with IL-6 cytokine concentration as outcome: Cauca

107 Finally, we identified the region in IL-6R that binds to CANDIS.

108 rkers rs1800797, rs1800796 and rs1800795; in IL-6R markers rs4075015, rs4601580, rs4645618, rs6687726

109 diverse oncogenic growth stimuli, including IL-6R, c-Src, Her2/Neu, is attenuated in cells without S

110 histochemistry and RT-PCR revealed increased IL-6R and decreased gp130 expression in amniochorion of

111 meningitis virus-specific Abs despite intact IL-6R expression in B cells.

112 we also observed suppression of interleukin (IL)6R, c-Myc, and reduced STAT3 phosphorylation.

113 the complex role of CD4(+) T cell-intrinsic IL-6R signaling, we induced nephrotoxic nephritis, a mou

114 we have reported the limitations of isolated IL-6R-alpha inhibition on dendritic cell-stimulated allo

115 ferring IL-6-responsiveness to cells lacking IL-6R such as synoviocytes.

116 oviding IL-6-responsiveness to cells lacking IL-6R.

117 Instead, we found full-length IL-6R on circulating microvesicles, establishing microve

118 chain of HCDR3 valine ties into site I like IL-6R Phe(279), whereas a LCDR1 tyrosine side chain occu

119 t the role of the 52-amino acid-residue-long IL-6R stalk region in shedding and signal transduction.

120 l and experimental peritonitis episodes lose IL-6R expression, and anti-CD3/CD28 Ab costimulation of

121 sians; however, in African-American maternal IL-6R marker rs4553185 associated with PTB (allele P = 4

122 d amino acids also abrogated ADAM10-mediated IL-6R shedding.

123 ite, also reduced ADAM10 and ADAM17-mediated IL-6R shedding, questioning the importance of cleavage s

124 t be regulating IL-6 signaling by modulating IL-6R stabilization and recycling.

125 25F10 is an anti-mouse IL-6R mAb that binds to both membrane-bound IL-6R and so

126 eukin-23 receptor (IL-23R) and IL-1R but not IL-6R signaling for their maintenance and pathogenicity.

127 the interactions of Phe(229) and Phe(279) of IL-6R.

128 espect to vIL-6 signalling in the absence of IL-6R but that retains the ability to mediate vIL-6 and

129 e to induce signaling even in the absence of IL-6R or EBI3.

130 ious studies that demonstrated activation of IL-6R by p28 (IL-30), new findings further suggest a com

131 Analysis of IL-6R and JAK1 expression in HCV patients by quantitativ

132 Appraisal of IL-6R expression on human and mouse T cells emphasized t

133 These data explain why blockade of IL-6R only achieves protection against EAE if used at th

134 by small interfering RNA or the blockade of IL-6R signaling exacerbated the TGF-beta-induced dysregu

135 the resultant conformation/dynamic change of IL-6R.

136 ands in the cytokine-binding domain (DII) of IL-6R.

137 amining the signaling pathways downstream of IL-6R in primary human T cells.

138 iRNA-449a and miRNA-107 target expression of IL-6R and JAK1, respectively, in vitro and also inhibit

139 duced by GATA-3 to inhibit the expression of IL-6R and STAT3.

140 (sIL-6R), but the cell surface expression of IL-6R and the mechanism of sIL-6R production are largely

141 n was enhanced in mice lacking expression of IL-6R by CD4(+) T cells and by treatment of wild-type mi

142 ted a possible role of tumoral expression of IL-6R in ovarian cancer.

143 two groups and found that high-expression of IL-6R mRNA in tumor tissues was a positive prognostic fa

144 acts in part by modulating the expression of IL-6R on T cells.

145 The expression of IL-6R was detected in 52.6% of hepatic CD3(+) T cells an

146 n in several models that the soluble form of IL-6R (sIL-6R) is involved in the recruitment of mononuc

147 otential clinical and biological function of IL-6R mRNA expression in ovarian cancer.

148 revealed that 25F10 interacts at site IIb of IL-6R but allows the binding of IL-6 to the IL-6R and th

149 ecall responses and to examine the impact of IL-6R blockade on Th17, Treg, follicular T helper (Tfh)

150 can function in human cells independently of IL-6R.

151 within site I and mimics the interactions of IL-6R Phe(229).

152 Simultaneously, high expression level of IL-6R mRNA correlates with better survival of patients w

153 sion, our results showed that mRNA levels of IL-6R in ovarian cancer was positively associated with b

154 al fibroblasts also express higher levels of IL-6R than do skin-derived cells.

155 Loss of IL-6R expression by activated T cells further suggests t

156 This reflected the loss of IL-6R expression by T cells over time.

157 ay infectious and allergic manifestations of IL-6R deficiency, and some of the skeletal abnormalities

158 Finally, systemic neutralization of IL-6R did not reduce arteriosclerotic thickening but red

159 les of putative cytokine-binding residues of IL-6R in ligand-induced functional complex formation are

160 hyperactivation of ADAM-mediated shedding of IL-6R as single substrate.

161 acetate-induced and spontaneous shedding of IL-6R resulting in the absence of sIL-6R in the culture

162 model, it is not ADAM17-mediated shedding of IL-6R within the pouch that orchestrates this inflammato

163 Blocking the IL-1R or IL-6R reversed cytokine impairment.

164 that could be reversed by blocking IL-1R or IL-6R.

165 ncomitant therapy with COX inhibitors and/or IL-6R antibodies might increase the clinical effect of p

166 nsion that was reversed by IL-22 deletion or IL-6R inhibition.

167 a novel molecular switch induced by EBI3 or IL-6R, respectively.

168 complexes consisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.

169 king mature IL-1beta, IL-6, IL-1R, MyD88, or IL-6R impair CD4(+) and CD8(+) T cell recovery and signi

170 experiments using ectopically overexpressed IL-6R and candidate proteases revealed major roles for t

171 he beta-receptor chains gp130 and Wsx-1, p28/IL-6R specifically recruits two gp130 beta-receptor chai

172 d baboon cells but not in pig cells (ie, pig IL-6R).

173 enograft because it is likely to bind to pig IL-6R, resulting in activation of pig cells.

174 Z and siltuximab do not cross-react with pig IL-6R and pig IL-6, respectively.

175 However, as we have shown previously, IL-6R can enhance vIL-6 signal transduction and can enab

176 ng mediated by IL-6 and its soluble receptor IL-6R (sIL-6R); by an antibody to the IL-6 receptor; or

177 onal amino acid change in the IL-6 receptor (IL-6R Asp358Ala; rs2228145) was significantly associated

178 Signaling by the interleukin 6 receptor (IL-6R) also activates STAT3 through Jak kinase.

179 ans-signaling via the soluble IL-6 receptor (IL-6R) and robustly support adult neurogenesis, specific

180 substrates of ADAM17 are the IL-6 receptor (IL-6R) and TNF-alpha.

181 s have been obtained with the IL-6 receptor (IL-6R) antagonist tocilizumab for the treatment of large

182 proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for inflammatory diseases

183 study evaluated the effect of IL-6 receptor (IL-6R) blockade with an antiYIL-6R monoclonal (mMR16-1)

184 binding to the cytokine with IL-6 receptor (IL-6R) by using side chains of two CDR residues filling

185 ng components of the interleukin-6 receptor (IL-6R) complex.

186 ical signaling after targeted IL-6 receptor (IL-6R) deletion in T cells eliminated pathogenic donor T

187 taneous reduction of interleukin-6 receptor (IL-6R) expression on myeloid progenitor cells by Delta-1

188 the epitope of human interleukin-6 receptor (IL-6R) for two adnectins with distinct affinities (Kd, A

189 58Ala variant in the interleukin-6 receptor (IL-6R) gene has been implicated in asthma, autoimmune an

190 A variant in the IL-6 receptor (IL-6R) gene increases asthma risk and is predicted to de

191 New therapies blocking the IL-6 receptor (IL-6R) have recently become available and are successful

192 ound and soluble forms of the IL-6 receptor (IL-6R) in processes called classic and trans-signaling,

193 body-mediated blockade of the IL-6 receptor (IL-6R) markedly reduces pathologic damage attributable t

194 wn-regulation of the interleukin 6 receptor (IL-6R) on naive CD4(+) T cells on the mRNA as well as on

195 Mice lacking IL-6 receptor (IL-6R) or IL-1 receptor 1 (IL-1R1) specifically on B cel

196 r, antibodies specific to the IL-6 receptor (IL-6R) or the gp130 subunit were capable of blocking the

197 the behavior of the specific IL-6 receptor (IL-6R) or the signal transducer gp130.

198 lex consisting of the cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-6R) and glycopr

199 IL6R coding change increases IL-6 receptor (IL-6R) shedding and promotes IL-6 transsignaling.

200 eceptor (IGF-1R) and interleukin-6 receptor (IL-6R) signaling (eg, IKK/NF-kappaB, PI-3K/Akt, and Raf/

201 )/IGF-1 receptor (IGF-1R) and IL-6 receptor (IL-6R) signaling cascades, antiapoptotic molecules (e.g.

202 or alpha (TNFalpha), interleukin 6 receptor (IL-6R), and epidermal growth factor receptor (EGFR) sign

203 ibodies directed at IL-6, the IL-6 receptor (IL-6R), and Janus kinase inhibitors.

204 naling via its membrane-bound IL-6 receptor (IL-6R), and trans-signaling via a naturally occurring so

205 e of monoclonal antibodies to IL-6 receptor (IL-6R), designed to block IL-6 pathways.

206 with the specific alpha-chain IL-6 receptor (IL-6R), is accessible and not occupied by gp130.

207 Expression of IL-6, IL-6 receptor (IL-6R), or glycoprotein 130, as well as IL-6 secretion,

208 nal antibody against interleukin-6 receptor (IL-6R), tocilizumab, prevented M2-differentiation.

209 urthermore, we identified the IL-6 receptor (IL-6R), which mediates IL-6-dependent STAT3 activation,

210 DES using a novel drug (anti-IL-6 receptor (IL-6R),Tocilizumab [TCZ]) + intravenous Ig (IVIg) to ass

211 not show activation of other IL-6 receptor (IL-6R)-mediated Janus kinase substrates, gp130, SHP-2, a

212 y the association of two IL-6.IL-6 receptor (IL-6R).gp130 trimers, with gp130 being the signal transd

213 s: by directly binding to the IL-6 receptor (IL-6R; CD126) or via trans-signaling, in which soluble I

214 t on the structurally related IL-6 receptor (IL-6R; gp80) subunit of the receptor-signal transducer c

215 ignaling membrane-bound IL-6 alpha-receptor (IL-6R) as an agonistic cytokine but also as a gp130 beta

216 ) and interleukin 6 (IL-6) and its receptor (IL-6R) in intercellular signaling pathways in the olfact

217 on that includes the gene for this receptor (IL-6R).

218 s conditioned by the transmembrane receptor (IL-6R) and homodimerization of gp130.

219 line, B9, and that the gp80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-signal transducer

220 ng these is tocilizumab (anti-IL-6 receptor [IL-6R]) which holds promise for modulating multiple immu

221 The resulting IL-6R/STAT3/miR-34a feedback loop was present in primary

222 hemical staining for IL-6R and CD31 revealed IL-6R expression on human endothelial cells within norma

223 nsive to requiring both IL-6 and soluble (s) IL-6R for activation.

224 otein and mRNA expression of sIL-6R, sgp130, IL-6R, and gp130.

225 sgp130) receptor to capture the IL-6/soluble IL-6R complex has shown promise for the treatment of rhe

226 hy results showed EGCG inhibits IL-6/soluble IL-6R-induced matrix metalloproteinase-2 activity in RA

227 High levels of both IL-6 and soluble IL-6R were found in AqH.

228 However, combinations of IL-6 and soluble IL-6R were highly effective inhibitors of T cell apoptos

229 nds to both membrane-bound IL-6R and soluble IL-6R with the unique property of specifically inhibitin

230 ells responded to trans-signaling by soluble IL-6R/IL-6 complexes, whereas no response was evident in

231 ane receptors, transsignaling (IL-6->soluble IL-6R->gp130) which activates any cell, and the recently

232 -signaling via a naturally occurring soluble IL-6R.

233 358Ala had increased serum levels of soluble IL-6R (P = 4 x 10(-14)), with homozygote carriers showin

234 ristics, whereas local regulation of soluble IL-6R activity might serve to maintain the cytokine prof

235 1 treatment combined with removal of soluble IL-6R using a dynamically fed culture system, reduces ma

236 acterized by excessive production of soluble IL-6R.

237 both with leukocyte numbers and i.p. soluble IL-6R (sIL-6R) levels.

238 APP gene induction with recombinant-soluble IL-6R linked to IL-6 cytokine (Hyper-IL-6) or with anoth

239 Elevated serum soluble IL-6R levels were associated with lower percent predicte

240 Serum soluble IL-6R levels were measured in subjects from SARP.

241 Moreover, we demonstrate that soluble IL-6R levels were higher in patients with AD than in con

242 amily members, OSM and IL-6 plus the soluble IL-6R (IL-6/R), prevent NMDA and glutamate-induced neuro

243 IL-6 trans-signaling via the soluble IL-6R (sIL-6R) plays an important role in the progressio

244 o induce p28-trans-signaling via the soluble IL-6R (sIL-6R), a characteristic property that was initi

245 PHX-induced generation of the soluble IL-6R by ADAM (a disintegrin and metallo) proteases enab

246 The soluble IL-6R is mainly generated by ADAM10- and ADAM17-mediated

247 leukocytes (classic), or through the soluble IL-6R, which binds the ubiquitously expressed gp130 (alt

248 uring trans-signaling, IL-6 binds to soluble IL-6R (sIL-6R), enabling activation of cells expressing

249 to soluble gp130 (sgp130) but not to soluble IL-6R (sIL-6R).

250 the classical membrane-bound versus soluble IL-6R signaling pathways.

251 26) or via trans-signaling, in which soluble IL-6R/IL-6 complexes bind to the signaling component CD1

252 iquitous IL-6 deletion or blockade, specific IL-6R deletion in T cells did not affect T follicular he

253 R-cKO), we demonstrated that T cell-specific IL-6R signaling is essential for viral control during pe

254 al tumors displayed upregulation of p-STAT3, IL-6R, and SNAIL and progressed to invasive carcinomas,

255 ependent on the IL-6 receptor alpha subunit (IL-6R, gp80) that is required for signaling by endogenou

256 ased 80-fold, and the IL-6 receptor subunits IL-6R alpha and gp130 were present in the adrenal cells.

257 sion, human osteoblasts express cell surface IL-6R, which is unable to transmit IL-6-induced signals

258 more promiscuous than that of hIL-6 but that IL-6R may play a role in vIL-6 signaling in vivo.

259 n on human and mouse T cells emphasized that IL-6R expression is closely linked with that of CCR7 and

260 e to support vIL-6 activity, indicating that IL-6R can form part of the signaling complex.

261 We posit that IL-6R cis-signaling is absolutely required for appropria

262 t population-based birth cohorts showed that IL-6R 358Ala specifically predisposes to the persistent

263 Although the IL-6R antagonist tocilizumab is approved for treatment o

264 or cross-talk between the BCR, TLR4, and the IL-6R or CD40.

265 nrelated 55-kDa, type I TNF receptor and the IL-6R, we propose that ARTS-1 may play an important role

266 Additionally, genes encoding the IL-6R and TGFbRII subunits were stably repressed, result

267 Both endothelial cell lines expressed the IL-6R and their stimulation with the exogenous ligand si

268 recruitment by IL-6 requires shedding of the IL-6R from infiltrating neutrophils.

269 re, we ruled out alternative splicing of the IL-6R mRNA as a potential source of circulating sIL-6R i

270 es demonstrate that antibody blockade of the IL-6R serves to recalibrate the effector and regulatory

271 ponse increase in the mRNA expression of the IL-6R signaling inhibitor protein suppressors of cytokin

272 Our findings underline a dual role of the IL-6R stalk region in IL-6 signaling.

273 Downstream of the IL-6R, HDAC inhibition was followed by a decrease in STA

274 set of NK cells expressed both chains of the IL-6R, IL-6 upregulated expression of the Th17-associate

275 via a membrane-bound or soluble form of the IL-6R, respectively.

276 st to the type I transmembrane proteins, the IL-6R, and IL-1RII, CANDIS does not bind the type II tra

277 he potential toxicity of drugs targeting the IL-6R.

278 Administration-approved Ab antagonist to the IL-6R (tocilizumab) attenuated the severity of influenza

279 IL-6 binds to the IL-6R alpha-chain (IL-6Ralpha) and signals via the signa

280 IL-6R but allows the binding of IL-6 to the IL-6R and the recruitment of gp130, forming a trimer com

281 y on the low-affinity binding of CNTF to the IL-6R.

282 ons and disrupts the binding of Stat3 to the IL-6R/gp130 peptide, GpYLPQTV-NH(2).

283 IL-6 can signal via the IL-6R complex composed of membrane-bound IL-6Ralpha (mIL

284 Here, we investigated the role of these IL-6R components in hypertension and vascular hypertroph

285 We show that acute signaling through IL-6R or CD40 integrates with chronic BCR-mediated ERK a

286 Binding of 25F10 to IL-6R prevented the formation of the hexameric complex o

287 d CV-5, however, lost the ability to bind to IL-6R.

288 n in hIL-6 participates in site I binding to IL-6R.

289 ypothesized that Arg(28) might contribute to IL-6R/CNTFR plasticity of CNTF.

290 t3 mutated at serine 727 and using truncated IL-6Rs suggested that the target of inhibition is contai

291 icular helper (Tfh) cell accumulation unless IL-6R-deficient T cells were competing with wild-type ce

292 Using IL-6R-deficient mice and recombinant tools that modulate

293 only CV-3 induced STAT3 phosphorylation via IL-6R.gp130.LIFR.

294 When IL-6R was blocked, LPS-responsive IkappaBepsilon(-/-) B

295 human IL-6 (hIL-6) signal transduction when IL-6R is coexpressed.

296 ly translated to experimental colitis, where IL-6R expression was suppressed in naive T cells, parall

297 s, we did not observe myoferlin binding with IL-6R.

298 t vIL-6, like hIL-6, can form complexes with IL-6R and gp130 but that the roles of putative cytokine-

299 te (HDM) or cockroach at day 0, treated with IL-6R inhibitors at day 13, and challenged with the same

300 the airways is attenuated by treatment with IL-6R inhibitors.