ライフサイエンスコーパス: IL

1 IL-10 from effector T cells signals to CD11c(+) myeloid

2 IL-10-oriented posttransplant response was associated wi

3 IL-1beta and IL-17 each suppressed Il25, Il33, and muc5a

4 IL-1beta is the most studied of the IL-1 family of cytok

5 IL-21 is a pleiotropic cytokine produced predominantly b

6 IL-23 and IL-1beta stimulation upregulates LAT1 expressi

7 IL-33 autoamplified itself and ST2 protein expression in

8 IL-33 treatment is therefore an attractive adjunctive st

9 IL-38 is the most recent member of the IL-1 superfamily

10 IL-4 treatment markedly reduced the infiltration of CD8(

11 IL-4Ralpha regulation of MMC9s is in part BATF-dependent

12 IL-6 overexpression promoted activation of CD4(+) T cell

13 IL-6, CRP and triglycerides are likely to be causally li

14 e measured soluble markers of interleukin 1 (IL-1) activation at 4 different time points before the c

15 nfected macrophages induce an interleukin-1 (IL-1)-dependent inflammatory cytokine response by recrui

16 Interleukin-10 (IL-10) is a dimeric cytokine with both immunosuppressive

17 ically, glucocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transcription

18 Interleukin 15 (IL-15) is an essential cytokine for the survival and pro

19 o proinflammatory cytokines: interleukin-17 (IL-17) and GM-CSF.

20 the individual roles of its ligands, IL-17A, IL-17F, and IL-17AF, are less clear.

21 nase Cyld prevents excessive interleukin 18 (IL-18) production in the colonic mucosa by deubiquitinat

22 ctivation leads to increased interleukin-18 (IL-18) production, whereas blockade of IL-18 receptor in

23 d consequent secretion of interleukin 1beta (IL-1beta).

24 larly, there were higher levels of IL-1beta, IL-6 and IL-8 cytokines were quantified in keratitis cau

25 sociated with death (interleukin [IL]-1beta, IL-6).

26 inflammation mediated by the IL-23/IL-1beta/IL-17 axis.

27 of low-dose recombinant human interleukin-2 (IL-2) combined with low-dose rapamycin to prolong graft

28 Interleukin-2 (IL-2) is a component of most protocols of adoptive cell

29 Interleukin-2 (IL-2) is a small alpha-helical cytokine that regulates i

30 Low-dose interleukin-2 (IL-2) represents a new therapeutic approach to regulate

31 ) failed to engraft even with interleukin-2 (IL-2) support.

32 ty of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loop involving inc

33 Interleukin 22 (IL-22) signals via both IL-22 receptor alpha1 (IL-22Ralp

34 The cytokine interleukin-22 (IL-22) is a critical regulator of epithelial homeostasis

35 ur studies revealed that the interleukin-22 (IL-22)/IL-17-producing ILCS was not altered during SIV i

36 ies revealed that the interleukin-22 (IL-22)/IL-17-producing ILCS was not altered during SIV infectio

37 trol skin inflammation mediated by the IL-23/IL-1beta/IL-17 axis.

38 immune-suppressive cytokine interleukin-27 (IL-27) is elevated in neonatal mice.

39 heterotrimeric receptor complex (IL-2Ralpha/IL-2Rbeta/gamma(c)).

40 5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

41 We found high amounts of interleukin 31 (IL-31) in skin wound tissue during the peak of itch resp

42 Interleukin-33 (IL-33) acts as an alarmin cytokine by alerting the syste

43 dherent eosinophils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

44 ated microglia in response to interleukin-4 (IL-4) stimulation.

45 cytokine activity, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological m

46 beta 1 (TGF-beta1) because of interleukin-4 (IL-4)- and signal transducer and activator of transcirip

47 anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected ear

48 ne activity, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological mechanis

49 t eosinophils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

50 In mice, Arg1 was upregulated in an IL-4/IL-13- and intestinal microbiota-dependent manner.

51 lux in immune control in the absence of IL-4/IL-13-dependent immune mechanisms.

52 nflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early afte

53 lminths) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils.

54 ) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils.

55 Circulating interleukin 6 (IL-6) levels surge during exercise and IL-6 favors exerc

56 F was not regulated by either interleukin 6 (IL-6) or IL-23, which are both potent inducers of GVHD-i

57 ncluding the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surface expression o

58 suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal ri

59 g the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surface expression of CD86

60 t form has been marked by elevation of IL-6, IL-10, TNF-alpha, and other cytokines and severe CD4(+)

61 NA levels of pro-inflammatory markers (IL-6, IL-1beta, COX-2 and TNF-alpha) decreased.

62 on of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

63 In addition, IL-17-induced neutrophil chemotaxis was dependent on CXC

64 Additionally, IL-6-deficient asthmatic mice exhibited reduced goblet c

65 sed by the commensal fungus Candida albicans IL-17R signaling is essential to prevent OPC in mice and

66 results in reduced production of TNF-alpha, IL-6, and IL-1beta and in limited M1 macrophage polariza

67 s and chemokines, including IL-1, TNF-alpha, IL-9, CXCL1, CCL2, and CCL5 in the bronchoalveolar lavag

68 -22) signals via both IL-22 receptor alpha1 (IL-22Ralpha1) and the common IL-10R2, belongs to the IL-

69 We generated an IL-10 mutant with enhanced affinity for its IL-10Rbeta r

70 In mice, Arg1 was upregulated in an IL-4/IL-13- and intestinal microbiota-dependent manner.

71 te the efficacy and safety of ixekizumab, an IL-17 inhibitor, in non-radiographic axial spondyloarthr

72 lli suppressed IL-6 (adjusted p < 0.001) and IL-8 (adjusted p = 0.0170) responses to G. vaginalis.

73 evels did not change, and sCD163, MCP-1, and IL-6 levels changed at a single time point.

74 cocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transcription, but also

75 CI, Salazar et al. show that while IL-17 and IL-9 induced distinct but complementary molecular pathwa

76 ry tumorigenic cytokines, such as IL-17A and IL-6, and increased STAT3 tyrosine phosphorylation.

77 al roles of its ligands, IL-17A, IL-17F, and IL-17AF, are less clear.

78 K cell responses were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restricted by hig

79 ect correlated with a reduction of IL-1A and IL-2, as well as Akt/mTOR phosphorylation.

80 ng 11 members, among which are IL-1alpha and IL-18.

81 IL-1beta and IL-17 each suppressed Il25, Il33, and muc5ac mRNA expres

82 inflammatory cytokines such as IL-1beta and IL-18 and concurrent late CAR T cell expansion character

83 on of proinflammatory cytokines IL-1beta and IL-18.

84 Interleukin (IL)-2 and IL-21 dichotomously shape CD8(+) T cell differentiation.

85 IL-23 and IL-1beta stimulation upregulates LAT1 expression and ind

86 ted human Th cells is modulated by IL-4, and IL-3 regulates the effector functions of Th2 cells.

87 ils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

88 y, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological mechanisms in asth

89 and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

90 ere were higher levels of IL-1beta, IL-6 and IL-8 cytokines were quantified in keratitis caused by Gr

91 y cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early after P. yoeli

92 n reduced production of TNF-alpha, IL-6, and IL-1beta and in limited M1 macrophage polarization.

93 ects of obesity on microglial activation and IL-1beta gene expression, and visualization of hippocamp

94 nflammatory mediators, such as TNF-alpha and IL-6.

95 tatin compound (simvastatin) blocked ATP and IL-33 release by lowering the expression of VDAC-1 in th

96 ventricles, inversely associated to CRP and IL (interleukin)-1 changes in acute infection patients.

97 in 6 (IL-6) levels surge during exercise and IL-6 favors exercise capacity.

98 Furthermore, IL-3R expressing and IL-3-secreting Th cells were high in house dust mite-all

99 n for 24 hours with anti-IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosino

100 Unexpectedly, the mRNA for GATA3 and IL-5 correlated better with mRNA for CD30, TNFR2, ICOS,

101 reactive protein (hsCRP), and both hsCRP and IL-6 decreased among participants receiving canakinumab

102 ative antitumor effect of LDH inhibition and IL-21.

103 I contains elevated amounts of D-lactate and IL-10 compared with control subjects, and bacterial lact

104 inhibition of Malat1 also suppresses Maf and IL-10 levels.

105 with rTSLP or vehicle, TSLPR(-/-) mice, and IL-33 receptor-deficient (ST2(-/-) ) mice were challenge

106 NLRP3 and IL-1beta were upregulated in the G, CP, and AgP groups c

107 T cells was dependent upon NFkappaB-p65 and IL-6 expression in dendritic cells (DCs), as well as ary

108 SP and IL-1beta levels were assayed in the culture medium by EL

109 In addition, TSLP and IL-33 synergistically promoted group 2 innate lymphoid c

110 tors thymic stromal lymphopoietin (TSLP) and IL-33 are consistently associated with adaptive Th2 immu

111 Anti-IL-10-treated nonhuman primates had similar overall dise

112 anti-IL-12/23 remained significant and anti-IL-6 antibodies became a trend after controlling for phy

113 nges in granulomas and lymph nodes from anti-IL-10-treated animals.

114 Effects of anti-IL-12/23 remained significant and anti-IL-6 antibodies b

115 Food and Drug Administration (FDA)-approved IL-1R antagonist; or parthenolide, a caspase-1 and nucle

116 kines, including 11 members, among which are IL-1alpha and IL-18.

117 -inflammatory tumorigenic cytokines, such as IL-17A and IL-6, and increased STAT3 tyrosine phosphoryl

118 Elevated inflammatory cytokines such as IL-1beta and IL-18 and concurrent late CAR T cell expans

119 reduced Bcl6 and PD-1 expression as well as IL-21 production by T(FH) cells, preventing proper spati

120 tion of IL-9 critically depends on autocrine IL-3 acting via the sustained activation of STAT5 on the

121 sults indicate that reducing IRI by blocking IL-1Rsignaling pathways with Anakinra or inflammasome ac

122 r of activated B cells inhibitor that blocks IL-1beta maturation.

123 Interleukin 22 (IL-22) signals via both IL-22 receptor alpha1 (IL-22Ralpha1) and the common IL-1

124 IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

125 IFN-gamma production, which was enhanced by IL-15.

126 potential but is impervious to inhibition by IL-18BP.

127 on activated human Th cells is modulated by IL-4, and IL-3 regulates the effector functions of Th2 c

128 eceptor alpha1 (IL-22Ralpha1) and the common IL-10R2, belongs to the IL-10 cytokine family, and is cr

129 gh-affinity heterotrimeric receptor complex (IL-2Ralpha/IL-2Rbeta/gamma(c)).

130 t mechanisms by which the enigmatic cytokine IL-17F contributes to host defense against fungi.

131 erein we identify the dual function cytokine IL-33 as an orchestrator of the glioblastoma microenviro

132 This process is inhibited by the cytokine IL-37.

133 the maturation of proinflammatory cytokines IL-1beta and IL-18.

134 ILC2-derived IL-13 was sufficient for RSV-driven AHR, since reconstit

135 Network analysis also suggested differential IL-6-related inflammatory programs in WT versus IRF3-KO

136 This TIC-driven, IL-33-TGF-beta feedforward loop could potentially be exp

137 3) production of anti-inflammatory effectors IL-10 and thioredoxin 1.

138 ee mice and found that aging led to elevated IL (interleukin)-6 levels and mitochondrial dysfunction,

139 These results suggest that endogenous IL-33 and its autoamplification of IL-33/ST2 pathway pla

140 Mechanistically, MAOA enhances IL-6 transcription through direct Twist1 binding to a co

141 veloped a therapeutic vaccine against equine IL-31 (eIL-31).

142 Alt-Ext or vehicle once or twice to evaluate IL-33 release and TSLP expression in the lung.

143 Seventeen out of 30 MeONPs induced excess IL-1beta production in THP-1 cells.

144 efv(M680I/M680I) FMF knock-in mice exhibited IL-1-dependent increased survival relative to wild-type

145 This population highly expressed IL-18R1 and promoted donor-specific antibodies in respon

146 e find that IL-2C targeting cells expressing IL-2 receptor beta cause an acute decrease in cellularit

147 in presymptomatic SOD1-G93A mice expressing IL-10 + M3 or IL-10 alone.

148 ls, they express the autocrine growth factor IL-2 which transforms them into rapidly dividing effecto

149 g higher performance differences between FIL/IL absorbents.

150 ed a kinetic control with highly viscous FIL/ILs, revealing higher performance differences between FI

151 Finally, IL-2/alphaIL-2 complex-expanded Treg cells could be reca

152 mpared to controls at baseline and following IL-33 stimulation.

153 lic dependency on the glycolytic pathway for IL-10 production, shifting from the fatty acid oxidation

154 Among HSPCs, we found that the receptor for IL-33, ST2, is expressed preferentially and highly on er

155 This reduced the input thresholds for IL-2 secretion in a sensitizer-like fashion.

156 Colon tumors from IL-17RD-deficient mice are characterized by a strong enr

157 Furthermore, IL-36R-mediated IL-22 production by CD4(+) T cells was d

158 Furthermore, IL-3R expressing and IL-3-secreting Th cells were high i

159 xpansion and cytokine production (IFN-gamma, IL-2, and TNF), with the highest median magnitude detect

160 ng MrgprA3, MrgprC11, histamine receptor H1, IL-31 receptor, 5-hydroxytryptamine receptor 1F, natriur

161 rulent strain induced less IL-10, but higher IL-12, in macrophages.

162 trate a previously unrecognized role of host IL-6 response in the regulation of lung inflammation dur

163 to this pleiotropic cytokine, including how IL-10 regulates basic processes of neural and adipose ce

164 e and immunostimulatory activities; however, IL-10-based therapies have shown only marginal clinical

165 S-induced macrophage activation by impairing IL-1beta production.

166 T1 expression and induces mTOR activation in IL-17(+) gammadelta and T(H)17 cells.

167 of wild-type ILC2 rescued RSV-driven AHR in IL-13-deficient mice.

168 ammals, but was not previously implicated in IL-17 signaling or nervous system function.

169 he activation marker CD86 and an increase in IL-10 production and was associated with a higher prolif

170 telet-adherent eosinophils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

171 ammatory cytokines and chemokines, including IL-1, TNF-alpha, IL-9, CXCL1, CCL2, and CCL5 in the bron

172 l proangiogenic factors in tumors, including IL-1beta and matrix metalloproteinase-9, and we found up

173 Estrogen receptor -alpha signaling increased IL-33 release and ILC2-mediated airway inflammation.

174 ol subjects, and bacterial lactate increases IL-10 production by human monocyte-derived macrophages.

175 d protein kinase-dependent Ripk1-independent IL-1 and tumor necrosis factor production, and were pron

176 strogen signaling increases allergen-induced IL-33 release, ILC2 cytokine production, and airway infl

177 OVA also induced IL-33 and ST2 protein expression.

178 expansion of peripheral and CNS-infiltrating IL-10(+) T cells.

179 Interleukin (IL)-13 is a type 2 cytokine with important roles in alle

180 Interleukin (IL)-1beta microinjected in the nucleus tractus solitarii

181 Interleukin (IL)-2 and IL-21 dichotomously shape CD8(+) T cell differ

182 e T cell proliferation, such as interleukin (IL)-15, have been explored as a means of boosting the an

183 like receptor (TLR)-related lnc interleukin (IL) 7 receptor (IL7R) were significantly reduced in peri

184 ginine in mice with deletion of interleukin (IL)12B, NLRP3, or IL18 and in mice given MCC950, a small

185 ese cells depends critically on interleukin (IL)-33 produced by local mesenchymal stromal cells (mSCs

186 ILC3) that continuously produce interleukin (IL)-22.

187 um albumin and iron], and serum interleukin (IL) 1beta were positively associated with DeltaCES-D(tot

188 Here, we show that interleukin (IL)-22, induced by colonization of the gut microbiota, i

189 Treatment with interleukin (IL)-22, a cytokine with multiple targets, ameliorated CX

190 th those associated with death (interleukin [IL]-1beta, IL-6).

191 Intranasal IL-4 treatment warrants further investigation as a clini

192 IL-10 mutant with enhanced affinity for its IL-10Rbeta receptor using yeast surface display.

193 The avirulent strain induced less IL-10, but higher IL-12, in macrophages.

194 ns, but the individual roles of its ligands, IL-17A, IL-17F, and IL-17AF, are less clear.

195 LA716 introgression line (IL) population using a combination of scanning electron

196 cluding NF-kB signaling, IL-6 signaling, LPS/IL-1-mediated inhibition of RXR Function, PI3K in B lymp

197 ly, mRNA levels of pro-inflammatory markers (IL-6, IL-1beta, COX-2 and TNF-alpha) decreased.

198 Furthermore, IL-36R-mediated IL-22 production by CD4(+) T cells was dependent upon NF

199 ited the secretion of inflammatory mediators IL-1beta and MCP-1.

200 We also adoptively transferred naive IL-4Ralpha(-/lox) or IL-4Ralpha(-/-) B cells into muMT(-

201 the C. elegans nervous system, and neuronal IL-17-MALT-1 signaling regulates multiple phenotypes, in

202 We find that neuronal IL-33 instructs microglial engulfment of the extracellul

203 l influx in immune control in the absence of IL-4/IL-13-dependent immune mechanisms.

204 d with WT mice, we show that the activity of IL-13 is dramatically augmented in SP-A(-/-) mice, which

205 Conversely, administration of IL-33 in healthy mice suppressed erythropoiesis, decreas

206 ndogenous IL-33 and its autoamplification of IL-33/ST2 pathway play an important role in the inductio

207 n-18 (IL-18) production, whereas blockade of IL-18 receptor in the brain helped protect against cereb

208 ion was restricted by high concentrations of IL-10.CONCLUSIONThis study demonstrates the induction of

209 day 3 to day 5-6, but the concentrations of IL-1beta for some embryos might double from day 3 to day

210 Depletion of IL-17A in vaccinated C57BL/6 mice prior to challenge abr

211 zumab treatment is supported by detection of IL-6 in pathogenic levels in all patients.

212 46 and DASA-58 suppressed the development of IL-17-producing T(H)17 cells but increased the generatio

213 everest form has been marked by elevation of IL-6, IL-10, TNF-alpha, and other cytokines and severe C

214 significant difference in the expression of IL-17 mRNA between OVA-treated skin of VAN and VAD mice.

215 Expression of IL-1beta and TNFalpha, which dramatically increased towa

216 lmost completely abrogates the expression of IL-3 in both cell types.

217 de the first evidence that the expression of IL-3R on activated human Th cells is modulated by IL-4,

218 o elevated chemokines and high expression of IL-6.

219 ned activation of STAT5 on the expression of IL-9.

220 lular signals constitutively, independent of IL-1beta stimulation, which was abrogated by deletion of

221 sprouting assays revealed that inhibition of IL-6 or STAT3 signaling decreases the vasculogenic poten

222 olled trial support further investigation of IL-1beta inhibition for treatment of large joint osteoar

223 Similarly, there were higher levels of IL-1beta, IL-6 and IL-8 cytokines were quantified in ker

224 rk, we hypothesized that increased levels of IL-27 predispose neonatal mice to more severe infection

225 Objective: To determine the mechanisms of IL-10 (interleukin-10) deficient-EPC-derived exosome dys

226 lture medium for chronic disease modeling of IL-13-induced airway hyper-responsiveness.

227 We investigated the therapeutic potential of IL-4 against fatal malaria in Plasmodium berghei ANKA-in

228 ever, selectively in BMMC, the production of IL-9 critically depends on autocrine IL-3 acting via the

229 This effect correlated with a reduction of IL-1A and IL-2, as well as Akt/mTOR phosphorylation.

230 his study, we investigated the regulation of IL-3R expression on human Th cells and also examined the

231 Physiological release of IL-17a by these cells was correlated with anxiety-like b

232 However, despite the important role of IL-1beta in controlling local and systemic inflammation,

233 To investigate the role of IL-1R signaling pathways during IRI, we treated syngenei

234 human Th cells and also examined the role of IL-3 in effector functions of these cells.

235 Here, we investigate the role of IL-31 in IBH of horses and developed a therapeutic vacci

236 ay a framework for understanding the role of IL-6 in the context of cancer research and COVID-19 and

237 lation and were the major cellular source of IL-22 binding protein (IL-22BP) at steady state.

238 -inflammatory properties similar to those of IL-37 but through different receptors.

239 , a murine model of MS, adoptive transfer of IL-10(+) regulatory B cells (B(regs)) has been shown to

240 own resistance by promoting upregulation of IL-7 receptor (IL-7R) expression.

241 Optimal NK cell responses were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restric

242 t to induce itching in a manner dependent on IL-31 expression.

243 blet cells do not depend on type I IFN or on IL-22 signaling, pathways responsible for protection aga

244 al changes were observed in UCH-L1, Iba-1 or IL-6 over 6 h.

245 regulated by either interleukin 6 (IL-6) or IL-23, which are both potent inducers of GVHD-induced co

246 Hepatic overexpression of Cxcl1 and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed m

247 ively transferred naive IL-4Ralpha(-/lox) or IL-4Ralpha(-/-) B cells into muMT(-/-) mice a day before

248 atic SOD1-G93A mice expressing IL-10 + M3 or IL-10 alone.

249 Increased permeability, IL-33 levels, type 2 innate lymphoid cell activation, an

250 rom RSV-infected infants showed elevated pro-IL-1beta mRNA and protein.

251 afollicular B helper T cells, which produced IL-10 and could play a prominent pathogenic role in SLE.

252 or cellular source of IL-22 binding protein (IL-22BP) at steady state.

253 by promoting upregulation of IL-7 receptor (IL-7R) expression.

254 However, recombinant IL-18 previously did not demonstrate efficacy in clinica

255 s antibiotic treatment, dramatically reduces IL-18 and intestinal inflammation.

256 oglia, not peripheral myeloid cells, release IL-1alpha ex vivo.

257 evolution, we engineered a 'decoy-resistant' IL-18 (DR-18) that maintains signalling potential but is

258 We also show that the SA-IL-4 fusion protein prevents immune-cell infiltration in

259 le lamin A/C to prevent cellular senescence, IL-6 expression, hyperosteoclastogenesis, and trabecular

260 Serum IL-27 levels continued to rise during infection.

261 gnaling pathways, including NF-kB signaling, IL-6 signaling, LPS/IL-1-mediated inhibition of RXR Func

262 Strikingly, IL-6 blockade attenuates disease only in mice treated wi

263 These results suggest IL-17RB can be a potential target for pancreatic cancer

264 Overall, lactobacilli suppressed IL-6 (adjusted p < 0.001) and IL-8 (adjusted p = 0.0170)

265 We find that IL-2C targeting cells expressing IL-2 receptor beta caus

266 Taken together, our data indicated that IL-25 signaling subverts the induction of protective imm

267 ger, supporting the recent observations that IL-6 and C-reactive protein could be used as markers for

268 We have reported that IL-18 plays an important role in radiation-induced injur

269 Last, we showed that IL-6 and C-reactive protein serum concentrations were hi

270 Collectively, our results suggest that IL-27 represents a therapeutic target to limit susceptib

271 The IL-23/T helper type 17 cell axis is a target for psorias

272 pared with IL-33(HET)/Tg+ mice, although the IL-33(KO)/Tg+ mice had significantly reduced levels of M

273 binding to a conserved E-box element at the IL-6 promoter.

274 to control skin inflammation mediated by the IL-23/IL-1beta/IL-17 axis.

275 we demonstrate a protective function for the IL-33-ST2 axis in bronchial epithelial repair, and impli

276 IL-1beta is the most studied of the IL-1 family of cytokines, including 11 members, among wh

277 We conclude that early blockade of the IL-1 receptor is therapeutic in acute hyperinflammatory

278 IL-38 is the most recent member of the IL-1 superfamily and has anti-inflammatory properties si

279 d loop involving increased expression of the IL-2 receptor alpha-subunit and activation of the transc

280 used mice deficient for either MyD88 or the IL-12Rbeta2 in the T cell lineage.

281 pha1) and the common IL-10R2, belongs to the IL-10 cytokine family, and is critically involved in tis

282 tion and disrupts STAT3 interaction with the IL-22 receptor.

283 ated that sorbitol is highly soluble in this IL.

284 pression of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

285 In addition to IL-10's classic inhibitory effects on myeloid cells, we

286 ted donor-specific antibodies in response to IL-18 in vivo.

287 By treating IL-4Ralpha(-/-) mice serially with anti-CCR3 Ab or intro

288 proteins of the stromal MAOA-induced Twist1/IL-6/STAT3 pathway in clinical specimens.

289 e structures in mouse macrophages undergoing IL-4-mediated fusion.

290 Upon IL-6 treatment, Endo-N and Endo-T cells displayed altere

291 were significantly altered in basal EV upon IL-13 treatment.

292 mma released by Vdelta2(+) cells upregulates IL-12 secretion by DCs in a positive feedback loop.

293 This suggests the possibility of using IL-6 or CRP level to guide escalation of treatment in pa

294 e of the JCI, Salazar et al. show that while IL-17 and IL-9 induced distinct but complementary molecu

295 As compared with IL-33(HET)/Tg+ mice, although the IL-33(KO)/Tg+ mice had

296 is, stimulation of nonlesional explants with IL-1beta resulted in transcriptomic and proteomic profil

297 Short-term incubation with IL-3 dose-dependently upregulated MRGPRX2 expression in

298 GF11 was found to cross-talk positively with IL-17A signalling.

299 chanistically, glucocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transc

300 tably, application of allergen together with IL-2/alphaIL-2 complexes induced expression of Treg mark

301 oducing a compound deficiency in CCR3 within IL-4Ralpha(-/-) mice, residual eosinophilia was ablated,