ライフサイエンスコーパス: IL-11

1 IL-11 and its receptor (IL11RA) are expressed specifical

2 IL-11 and its receptor, IL-11Ra, are expressed in human

3 IL-11 and PGs mediate LPS-induced bone resorption by enh

4 IL-11 at 0.1 and 10 ng/ml induces tyrosine phosphorylati

5 IL-11 but not IL-6 levels were found previously to be up

6 IL-11 can reduce tissue injury in animal models of infla

7 IL-11 caused airway fibrosis with the enhanced accumulat

8 IL-11 did not cause a comparable decrease in mucus hyper

9 IL-11 does not activate NF-kappaB nor does it inhibit NF

10 IL-11 has no effect on T cell activation marker, effecto

11 IL-11 increased the numbers of spinal cord inflammatory

12 IL-11 induced a shift of hsp25 to Triton x-100 insoluble

13 IL-11 induces hsp25 in an intestinal epithelial-specific

14 IL-11 induction of hsp72 and hsp25 was determined by imm

15 IL-11 is a pleiotropic cytokine that induces tissue remo

16 IL-11 is the highest upregulated cytokine in the sera an

17 IL-11 protects barrier integrity during oxidant stress,

18 IL-11 receptor (IL-11R) activation was determined using

19 IL-11 signaling may represent a therapeutic avenue to re

20 IL-11 therefore drives a pathway that enhances HSPC radi

21 IL-11 up-regulates the expression of survivin, a cytopro

22 IL-11 was administered daily by enteric, coated multipar

23 IL-11 was induced in human astrocyte cultures by the cyt

24 IL-11(+)CD4(+) cells accumulate in the cerebrospinal flu

25 IL-11, a gp130-signaling cytokine, is protective in seve

26 IL-11, IL-17, RANTES, and IL-6 concentrations were asses

27 IL-11, IL-6, and RANTES concentrations were significantl

28 IL-11-induced cytoprotection is protein synthesis depend

29 igate the contributions that interleukin 11 (IL-11) and IL-13 might make to airway remodeling respons

30 emonstrated that blocking of interleukin 11 (IL-11) by systemic administration of anti-IL-11 antibodi

31 nd isolated a mimic motif of interleukin 11 (IL-11) from prostate biopsies after an i.v. administrati

32 response-betacellulin (BTC), interleukin 11 (IL-11), and IL-17F-that caused time-dependent induction

33 ys 1 and 15, with or without interleukin 11 (IL-11; 15 microg/kg per day on days 3 to 28), with assig

34 Neurotrophic Factor (CNTF), Interleukin-11 (IL-11) and Cardiotrophin (CT-1).

35 n MS lesions, and identified interleukin-11 (IL-11) as an astrocyte-derived factor that potentiates o

36 The mechanisms of interleukin-11 (IL-11) cytoprotection in intestinal epithelial injury ar

37 Interleukin-11 (IL-11) is a thrombopoietic cytokine that attenuates post

38 Interleukin-11 (IL-11) is a unique thrombopoietic growth factor which ca

39 blasts, that upregulation of interleukin-11 (IL-11) is the dominant transcriptional response to TGFbe

40 CL2 target genes include the interleukin-11 (IL-11) receptor Il11ra1, and recombinant IL-11 enhances

41 he multifunctional cytokine, interleukin-11 (IL-11), ameliorates the intestinal radiation response, b

42 howed that the expression of interleukin-11 (IL-11), an anti-inflammatory cytokine mainly active on m

43 ber of this cytokine family, interleukin-11 (IL-11), and components of its receptor (interleukin-11 r

44 beta), interleukin-6 (IL-6), interleukin-11 (IL-11), oncostatin M (OSM), and leukemia inhibitory fact

45 te-colony stimulating factor (G-CSF), IL-33, IL-11, IL-1alpha, and IL-1beta.

46 tem cell factor (SCF), interleukin 6 (IL-6), IL-11, and Flt3-l inhibited myeloid differentiation and

47 family, which includes interleukin 6 (IL-6), IL-11, CNTF, and LIF, and the leptin receptor is homolog

48 cells were cultured in interleukin-6 (IL-6), IL-11, granulocyte colony-stimulating factor (G-CSF), st

49 tem cell factor (SCF), interleukin-6 (IL-6), IL-11, IL-1beta, IL-8, and tumor necrosis factor-alpha l

50 e cytokines, including interleukin 6 (IL-6), IL-11, IL-27, oncostatin M (OSM), and leukemia inhibitor

51 m-free medium containing interleukin (IL)-6, IL-11, granulocyte colony-stimulating factor, stem cell

52 as serum amyloid A3, C3, interleukin (IL)-6, IL-11, IL-1 receptor antagonist, vascular endothelial gr

53 emokines and growth factors, including IL-6, IL-11 and IL-23 as well as CCL2, CCL5, CXCL7, CXCL5, ICA

54 on of three gp130-signaling cytokines, IL-6, IL-11, and leukemia inhibitory factor (LIF), as well as

55 s were cultured in interleukin (IL)-3, IL-6, IL-11, and steel factor for 0 to 48 h and tested for eng

56 ubstitution is associated with loss of IL-6, IL-11, IL-27, and OSM signaling but a largely intact LIF

57 tralized by an excess of antibodies to IL-6, IL-11, leukemia inhibitory factor (LIF), gp130, stromal

58 nctionally related proteins, including IL-6, IL-11, leukemia inhibitory factor (LIF), oncostatin M (O

59 ction and DN for cellular responses to IL-6, IL-11, LIF, and OSM.

60 ce a novel peptide, distinct from TPO, IL-6, IL-11, LIF, other gp130-associated interleukins, and SDF

61 Plasma and GCF IL-1beta, IL-6, IL-11, OSM, and LIF levels were analyzed by enzyme-linke

62 QRT-PCR validation of interleukin (IL)-8, IL-11, and suppressor of cytokine signaling 2 (SOCS2) me

63 In addition, IL-11 did not augment IFN-gamma production demonstrating

64 In addition, IL-11 treatment did not affect cytolytic effector functi

65 In addition, IL-11 was shown to inhibit asthma-like inflammation whil

66 se results indicate that orally administered IL-11 may preserve epithelial cell integrity in the pres

67 It was hypothesized that orally administered IL-11 would prevent mucosal damage and protect against m

68 onsecutive secondary cellular response after IL-11 induction by LfcinB-ERK-AP-1 axis in human adult a

69 Although IL-11 does not alter class I MHC complex molecule expres

70 Administration of an IL-11-neutralizing antibody abolished the renal protecti

71 sm, whereby LfcinB induces TIMP-1 through an IL-11-dependent pathway involving transcription factor A

72 i-inflammatory cytokines including IL-10 and IL-11 as well as FOXP3 were upregulated in the colon by

73 IL-11 and the concentration of the IL-17 and IL-11/IL-17 ratio were significantly lower in the GAgP g

74 also revealed that betacellulin, IL-17, and IL-11 cytokines have the novel property of enhancing the

75 levated expression of interleukin (IL)-6 and IL-11 and activation of the STAT3 and NF-kappaB signalin

76 Elevated levels of IL-6 and IL-11 are associated with multiple myeloma, rheumatoid a

77 enocopies through impairment of the IL-6 and IL-11 response pathways.

78 s and fibroblasts respond poorly to IL-6 and IL-11.

79 ytokines, including interleukin-6 (IL-6) and IL-11, did not induce platelet production in thrombocyto

80 ng factor (G-CSF), interleukin-6 (IL-6), and IL-11 production by bone marrow stromal cells.

81 e present data, elevated IL-1beta, IL-6, and IL-11 GCF levels, but not plasma levels, are suggested a

82 significantly higher GCF IL-1beta, IL-6, and IL-11 levels when compared with the H group (P <0.05).

83 in the presence of thrombopoietin, IL-6, and IL-11 resulted in the development of large, polyploid me

84 ar endothelial cell growth factor, IL-6, and IL-11 were decreased in the bronchoalveolar lavage fluid

85 pecifically inhibits the growth of IL-6- and IL-11-dependent cell lines, most likely by interfering w

86 nalyzed by Q-PCR, and expression of IL-8 and IL-11 was analyzed by ELISA.

87 xpression of inflammatory mediators IL-8 and IL-11.

88 es are in secreted proteins, IL-6, IL-8, and IL-11 and chemokines CXCL2 and CXCL5, or genes associate

89 TNF-alpha and IL-11 levels were 2.5-3 times higher in T47D conditioned

90 pecimens, where immunoreactive TNF-alpha and IL-11 were readily detectable in malignant epithelial ce

91 s via the action of cytokines (TNF-alpha and IL-11) secreted by the malignant epithelial cells to inh

92 fect on expression of CXCL10, TGF-beta1, and IL-11 and exacerbated the rapid up-regulation of mRNAs e

93 phic factor, leukemia inhibitory factor, and IL-11 have been identified as oligodendrocyte growth fac

94 ified as oligodendrocyte growth factors, and IL-11 is also strongly immunoregulatory, but their under

95 All groups had similar LIF and IL-11 total amounts (P >0.008).

96 ors for leukemia inhibitory factor (LIF) and IL-11 is essential for embryo attachment and decidualiza

97 (OSM), leukemia inhibitory factor (LIF), and IL-11, have fibrogenic features.

98 GCF IL-6, IL-1beta, OSM, LIF, and IL-11 levels were analyzed by enzyme-linked immunosorben

99 [OSM], leukemia inhibitory factor [LIF], and IL-11).

100 were detected among IL-6, IL-1beta, OSM, and IL-11 total amount in GCF and clinical parameters (P <0.

101 f A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci.

102 factor (TNF) monoclonal antibody (MAb), anti-IL-11 MAb, or saline control.

103 1 (IL-11) by systemic administration of anti-IL-11 antibodies attenuates severity of Mycobacterium tu

104 ce were then treated with injections of anti-IL-11 monoclonal antibody (MAb), indomethacin, or phosph

105 step toward clinical evaluation of the anti-IL-11 therapy for tuberculosis.

106 The increase was reduced by 37% with anti-IL-11 MAb and by 46% with indomethacin.

107 Rp55(-/-)-IL-1RI(-/-) mice treated with anti-IL-11 MAb or indomethacin, respectively.

108 specific CD4+ T lymphocytes and CD11c+ APCs, IL-11 treatment resulted in a significant decrease in T

109 inant inflammatory disorders such as asthma, IL-11 is simultaneously induced.

110 ural mechanisms of complex formation between IL-11 and IL-11Ralpha differ substantially from those pr

111 However, the relationship(s) between IL-11 and IL-13 in these responses has not been defined,

112 +) cells, we propose that cross-talk between IL-11(+)CD4(+) and Th17 cells may play a role in the inf

113 antiapoptotic effects of IL-11 on OPCs, but IL-11 induced apoptosis in the presence of Stat3 silenci

114 The induction of hsp25 by IL-11 confers epithelial-specific cytoprotection that is

115 4) that encodes novel transcripts induced by IL-11 in mouse 3T3 L1 cells.

116 apoptosis and necrosis that is inhibited by IL-11 and other interventions.

117 , LPS-induced bone resorption is mediated by IL-11 and PGs, while at high doses of LPS (500 microg/mo

118 of LPS (500 microg/mouse), it is mediated by IL-11, PGs, IL-1, and TNF signaling.

119 n-gamma levels were significantly reduced by IL-11 treatment (2477 vs. 0 pg/mL, P<.01).

120 ich specifically inhibits gp130 signaling by IL-11 but not by other IL-6 type cytokines.

121 Transgene- and CC10-IL-11 transgene+ mice had comparable levels of circulati

122 erexpressed in a lung-specific fashion (CC10-IL-11) with that in transgene- wild-type littermate cont

123 In contrast, OVA challenge in CC10-IL-11 animals elicited impressively lower levels of tiss

124 Among these cytokines, we found that CNTF, IL-11, and Clcf1/Crlf1a can stimulate optic axon regrowt

125 In contrast, IL-11 augmented caspase activation and apoptosis in cult

126 In contrast, IL-11 blocking antibodies increased Lyme arthritis.

127 In contrast, IL-11 stimulated A1, diminished the toxic effects of hyp

128 Conversely, IL-11 strongly reduced apoptosis and potentiated mitosis

129 AGGSC) bound specifically to a corresponding IL-11 receptor (IL-11Ralpha).

130 godendrocyte progenitor cell (OPC) cultures, IL-11 restricted caspase 9 activation and apoptosis, and

131 ium in response to the inflammatory cytokine IL-11, which is required for the growth of gastric cance

132 radiation resistance identified the cytokine IL-11 as being critical for the ability of Lnk(-/-) HSPC

133 enetic ablation of signaling by the cytokine IL-11, which promotes gastric tumorigenesis via STAT3.

134 induction of an anti-inflammatory cytokine, IL-11.

135 Gene microarray analysis revealed decreased IL-11 expression in TMED3-knockdown cells.

136 d in the GAgP group because of the decreased IL-11 levels.

137 udy suggests that administration of low-dose IL-11 (10 microg/kg/d) can raise platelet counts without

138 We, therefore, initiated a study of low-dose IL-11 (starting dose, 10 microg/kg/d).

139 Dysregulated IL-11 signaling has been implicated in several diseases,

140 ine Lyme carditis was not affected by either IL-11 or IL-11 antibodies.

141 HUVECs express IL-11 receptor alpha-chain and gp130.

142 Similarly, neutralizing antibodies for IL-11 reduced the tumor size.

143 findings suggest an obligate requirement for IL-11 signaling via constitutive pS-STAT3 in Helicobacte

144 Compared with the placebo group, IL-11-treated rats retained mucosal mass and had prolong

145 Human IL-11 causes rapid (2-10 min) tyrosine phosphorylation o

146 Intradermal injection of human IL-11 (500 ng/day) delays the time course of graft micro

147 rpose was to compare concentrations of human IL-11 and IL-17 within healthy and diseased human gingiv

148 f human IL-11Ralpha and a structure of human IL-11 that reveals previously unresolved detail.

149 Treatment with recombinant human IL-11 (25 microg/kg/day subcutaneously) was initiated an

150 Recombinant human IL-11 (rhIL-11; 2 mg/kg/d) or vehicle was given through

151 uction either by exogenous recombinant human IL-11 or by autocrine production of IL-11 in cells cultu

152 jected subcutaneously with recombinant human IL-11 or control diluent twice daily, from 2 days before

153 Furthermore, we have identified IL-11 as a new Th17-promoting cytokine, because it induc

154 These data are the first to implicate IL-11 in oligodendrocyte viability, maturation, and myel

155 Importantly, IL-11 was detected most readily in tissues from asthmati

156 In IL-11 signaling, wild-type Lnk suppresses tyrosine phosp

157 rfusion injury in wild-type mice, but not in IL-11 receptor-deficient mice.

158 in HK-2 cells and wild-type mice, but not in IL-11 receptor-deficient or renal proximal tubule A1 ade

159 duction of an inflammatory program including IL-11 production and activation of the JAK/STAT3 pathway

160 The induced IL-11 functions as an anti-inflammatory and chondroprote

161 s BHLHE41 expression which, in turn, induces IL-11, a member of the IL-6 cytokine family.

162 ammatory (IL-6, IL-8) and anti-inflammatory (IL-11) ILs, along with SOCS2, shows that LPA transiently

163 Our results introduce IL-11 as a new cytokine that plays a role in the autoimm

164 o show that both IL-11Ralpha and its ligand, IL-11, are specifically up-regulated in human metastatic

165 y identified expression of the family member IL-11 in active MS plaques.

166 Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory

167 In A1-null mice, IL-11-induced protection, survival advantage, and Bcl-2

168 cule expression, pretreatment with 0.5 ng/ml IL-11 partially protects HUVECs against lysis by allospe

169 are phosphorylated in response to 0.3 ng/ml IL-11 with maximal activation at 30 ng/ml IL-11.

170 ml IL-11 with maximal activation at 30 ng/ml IL-11.

171 onclude that in this human transplant model, IL-11 exerts a cytoprotective rather than anti-inflammat

172 Moreover, IL-11 activates STAT3 signaling pathway to critically up

173 s an effective tool for inhibition of native IL-11 activity in vivo.

174 ed by the IL-6-related cytokine OSM, but not IL-11 or LIF.

175 The ability of IL-11 to activate STAT3 in prostate-derived cells may be

176 Protective actions of IL-11 are most pronounced on day 15.

177 Smad-dependent transcriptional activation of IL-11 and its overexpression in bone-metastatic cells.

178 Very little is known about the activity of IL-11 in patients with bone marrow failure states.

179 inhibitor and through exogenous addition of IL-11 that the host responses to the 6B ST90 and TIGR4 s

180 Addition of IL-11, but not TPO, to NKCM-containing cultures resulted

181 Administration of IL-11 at the time of clinical onset of RREAE induced an

182 Administration of IL-11 was associated with increased production of mRNA f

183 e achieved by intraluminal administration of IL-11.

184 ng as a high-affinity specific antagonist of IL-11-mediated signaling.

185 The total amount and concentration of IL-11 and the concentration of the IL-17 and IL-11/IL-17

186 Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjace

187 TAT3- and MAPK-activating) concentrations of IL-11 confer resistance to immune-mediated injury in cul

188 ermine the role and relative contribution of IL-11 and prostaglandin(s) (PG[s]) in LPS-induced bone r

189 ia, since theoretically there is a danger of IL-11 stimulating the immune system by up-regulating the

190 from mice with RREAE after a single dose of IL-11 induced severe RREAE with increased accumulation o

191 ted mice, suggesting a predominant effect of IL-11 on the innate immune response.

192 d largely abrogates the protective effect of IL-11.

193 Importantly, the effects of IL-11 are achieved via a combination of immunoregulation

194 study, we demonstrate that these effects of IL-11 are mediated via differential regulation of apopto

195 by contributing to the protective effects of IL-11 in models of intestinal epithelial injury.

196 tat3 exacerbated the proapoptotic effects of IL-11 on DCs, whereas they were ablated in Stat1(-/-) cu

197 Stat1 enhanced the antiapoptotic effects of IL-11 on OPCs, but IL-11 induced apoptosis in the presen

198 To characterize the effects of IL-11 on Th2 tissue inflammation, we compared the inflam

199 n important role in mediating the effects of IL-11 under hypoxic conditions.

200 Side effects of IL-11 were mild (peripheral edema, n = 7; conjunctival i

201 demonstrating that the inhibitory effects of IL-11 were not due to a shift toward Th1 inflammation.

202 eveals key determinants of the engagement of IL-11 by IL-11Ralpha that may be exploited in the develo

203 inant amelogenin did not alter expression of IL-11 and PRG4.

204 ladenosine (CCPA), induced the expression of IL-11 mRNA and protein in an extracellular signal-regula

205 his hypothesis we compared the expression of IL-11, IL-11Ralpha, and gp130 in lungs from wild-type mi

206 vely increased BHLHE41 induces expression of IL-11.

207 blished the recombinant W147A mutant form of IL-11 in an optimized Escherichia coli expression system

208 We hypothesized that this mutant form of IL-11 may serve as an effective tool for inhibition of n

209 TGF-beta1 provoked a significant increase of IL-11 and PRG4 expression of oral fibroblasts when seede

210 stases and is essential for the induction of IL-11, a gene implicated in bone metastasis in this mous

211 n fibrosis and we propose that inhibition of IL-11 is a potential therapeutic strategy to treat fibro

212 Therefore, inhibition of IL-11 prevents fibroblast activation across organs and s

213 Levels of IL-11 and IL-17 in GCF samples were evaluated using enzy

214 ncogenic Smo, SmoM2, have elevated levels of IL-11, IL-11Ralpha, and STAT3 phosphorylation at Tyr(705

215 also exhibited an increase in mRNA levels of IL-11, RANTES, TNFalpha, TNFbeta, and MIP-1alpha.

216 l gene expression and a critical mediator of IL-11- and VEGF-induced cytoprotection.

217 critical regulator of HALI and a mediator of IL-11-induced cytoprotection.

218 eripheral circulation, and the percentage of IL-11(+)CD4(+) cells is significantly increased in CIS p

219 nt human IL-11 or by autocrine production of IL-11 in cells cultured under hypoxic conditions.

220 The pathological relevance of IL-11 signaling to osteoarthritis is evidenced by signif

221 et al. provides new insight into the role of IL-11 and its glycoprotein 130 (gp130) receptor in infla

222 These results reveal a central role of IL-11 in fibrosis and we propose that inhibition of IL-1

223 ouse studies have confirmed a causal role of IL-11 in the exacerbation of relapsing-remitting experim

224 man cancers; however, the functional role of IL-11 in tumor progression is not known.

225 ses has not been defined, and the role(s) of IL-11 in the genesis of the tissue effects of IL-13 has

226 cells represent a predominant cell source of IL-11 in the peripheral circulation, and the percentage

227 nstrate that IL-13 is a potent stimulator of IL-11 and IL-11Ralpha.

228 n of CCPA in mice induced renal synthesis of IL-11.

229 ed with IL-4 or IL-13, but not with IL-10 or IL-11, became protected from killing by complement and a

230 carditis was not affected by either IL-11 or IL-11 antibodies.

231 11 but was significantly increased by TNF or IL-11 inhibition.

232 lpha and interferon-gamma revealed that oral IL-11 reduced but did not prevent increased expression o

233 cytokines, IL-6, sIL-6R, oncostatin M (OSM), IL-11, and leukemia inhibitory factor (LIF) was determin

234 cytokine family, including oncostatin (OSM), IL-11, ciliary neurotrophic factor (CNTF), and leukemia

235 pression of the TGF-beta target genes PTHrP, IL-11, CTGF, and RUNX2.

236 11 (IL-11) receptor Il11ra1, and recombinant IL-11 enhances crypt cell regenerative potential.

237 otic, prorestitution genes (Bcl-x(L), RegIV, IL-11, IL-18), and basal rates of epithelial apoptosis a

238 Similarly, CCPA did not induce renal IL-11 expression or protect against renal ischemia-reper

239 ation of the effect of recombinant human (rh)IL-11 on vWf and factor VIII (FVIII) secretion.

240 In MS tissue samples, IL-11 was expressed by reactive astrocytes, with express

241 Serum IL-11 levels are significantly increased during clinical

242 Similarly, IL-11 neither induces E-selectin or ICAM-1 nor blocks in

243 and facilitates colonization by stabilizing IL-11 mRNA, thus promoting both early and late steps of

244 These studies demonstrate that IL-11 selectively inhibits Ag-induced eosinophilia, Th2

245 Importantly, we also found that IL-11 treatment was associated with significantly increa

246 We hypothesized that IL-11, signaling via the IL-11Ralpha-gp130 receptor comp

247 n intestinal epithelia, we hypothesized that IL-11-conferred cytoprotection is mediated by inducible

248 The results indicate that IL-11 down-regulates cytokine production but does not ex

249 These data indicate that IL-11-mediated induction of JAK/STAT3 is critical in gas

250 Regression analyses indicated that IL-11 was independently predictive of CR but not surviva

251 Collectively, these data reveal that IL-11 regulates inflammatory demyelination via a unique

252 Ag recall assays revealed that IL-11 induces IL-17A(+), GM-CSF(+), and IL-21(+)CD4(+) m

253 We show that IL-11 and IL-11Ralpha form a 1:1 complex with nanomolar

254 Our data show that IL-11 directly attenuates IL-1-mediated catabolic and in

255 In this study, we show that IL-11 regulates the clinical course and neuropathology o

256 s of GVL and GVHD in this system showed that IL-11 selectively inhibited CD4-mediated GVHD, while ret

257 These results suggest that IL-11 might serve as a biomarker of early autoimmune res

258 This suggests that IL-11 elaboration is, in part, an attempt at airway heal

259 The IL-11 effect on hsp25 distribution was characterized by

260 The IL-11/IL-17 axis and the link between IL-17 and neutroph

261 The IL-11/IL-17 ratio was decreased in the GAgP group becaus

262 signaling activation may be mediated by the IL-11/IL-11Ralpha signaling axis.

263 Here, we identify the IL-11 receptor alpha subunit (IL-11Ralpha) as a cell sur

264 the vehicle group versus 4.0 +/- 0.3 in the IL-11 group; P = 0.001), mucosal surface area loss (0.2

265 The substitution W147A in the IL-11 molecule creates the form of cytokine capable to d

266 odeling that was similar to that seen in the IL-11 transgenic mice.

267 induce differentiation of naive cells in the IL-11-secreting CD4(+) cells, we propose that cross-talk

268 Conversely, Gkn2 knockout in the IL-11/STAT3-dependent gp130F/F GC model caused tumorigen

269 Remodelling of the IL-11 locus facilitates p65 access to three NF-kappaB si

270 t of strategies to modulate formation of the IL-11-IL-11Ralpha complex.

271 d be investigated to clarify the role of the IL-11/IL-17 axis and its balance and imbalance in the pa

272 We also demonstrated that the IL-11 phage mimic (displaying the cyclic nonapeptide CGR

273 Thus, the IL-11 receptor system is up-regulated in prostate carcin

274 d of c-Fos and JunD, which transactivate the IL-11 gene.

275 ls leads to chromatin remodelling within the IL-11 promoter in a KDM6B-dependent manner, where KDM6B

276 e that TMED3 promotes HCC metastasis through IL-11/STAT3 signaling.

277 ilineage response (to IL-11 alone, n = 1; to IL-11 plus G-CSF and erythropoietin, n = 1).

278 per day on days 3 to 28), with assignment to IL-11 treatment made randomly.

279 sting that mutations in gp130 are leading to IL-11-like signaling.

280 domain that is phosphorylated in response to IL-11 stimulation.

281 -11, and two had a multilineage response (to IL-11 alone, n = 1; to IL-11 plus G-CSF and erythropoiet

282 of 16 patients showed a platelet response to IL-11, and two had a multilineage response (to IL-11 alo

283 on primary response gene 88 (MyD88) and Toll-IL-11 receptor domain containing adaptor protein (TIRAP)

284 uated the function of renal proximal tubular IL-11, a clinically approved hematopoietic cytokine, in

285 gest that induction of renal proximal tubule IL-11 is a critical intermediary in A1 adenosine recepto

286 elicited by OVA in sensitized mice in which IL-11 is overexpressed in a lung-specific fashion (CC10-

287 11 (all cytogenetic groups), and for GO with IL-11, less than 0.25 for AC groups and about 0.50 for N

288 without IL-11 and 9 of 25 (36%) for GO with IL-11.

289 relia burgdorferi-infected mice treated with IL-11 developed less arthritis than did control animals.

290 Conversely, wild-type mice treated with IL-11 displayed milder clinical signs and neuropathology

291 In cultures treated with IL-11, we observed a significant increase in oligodendro

292 Brief treatment with IL-11 shortly after BMT may therefore represent a novel

293 abilities were less than 0.02 for GO without IL-11 (all cytogenetic groups), and for GO with IL-11, l

294 (CR) rates were 2 of 26 (8%) for GO without IL-11 and 9 of 25 (36%) for GO with IL-11.

295 ior with IA compared with GO with or without IL-11 (P =.03).

296 nclude that survival with GO with or without IL-11 is likely longer than with IA.

297 terior probabilities that GO with or without IL-11 produced longer survival than IA, after accounting

298 evidence to suggest that GO with or without IL-11 should be used instead of IA in older patients wit

299 s) arising because IA and GO with or without IL-11 were not arms of a randomized trial.

300 We compared GO with or without IL-11 with idarubicin plus cytosine arabinoside (IA), as