ライフサイエンスコーパス: IL

1 IL-15 equally sustains wild-type and Il7ra(-/-) ILC surv

2 IL-15 KO mice showed improved survival, attenuated hypot

3 IL-18 activity is modulated in vivo by its naturally occ

4 IL-19, a member of the IL-10 cytokine family that signal

5 IL-1alpha was directly involved in IL-8 production and l

6 IL-22 treatment does not affect the flux of uncharged ma

7 IL-27 is predominantly synthesized by mononuclear phagoc

8 IL-27 suppressed osteoclastogenesis in an Egr-2-dependen

9 IL-33 dysregulated lung Treg cells and impaired immunolo

10 IL-37 is a novel pro-angiogenic cytokine that potently p

11 IL-6 signaling was increased by Gab2 overexpression and

12 IL-7 therapy has been evaluated in patients who do not r

13 pression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

14 the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

15 SCs with monocyte chemoattractant protein-1, IL-6, IL-1beta, and is associated with increased MyoD ex

16 STAT3 to regulate the balance between IL-12/IL-23 subunits causing a cytokine milieu rich in IL-23 t

17 ary human epithelial cells exposed to IL-13, IL-17A, or both.

18 nregulation of Th17-associated genes IL-17A, IL-22, and retinoic acid-related orphan receptor gammat.

19 haride and NLRP3-mediated interleukin-1beta (IL-1beta) secretion.

20 pro-inflammatory cytokine interleukin-1beta (IL-1beta).

21 atory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), and attenuated the wasting syndro

22 activated by the endogenous cytokines IL-2, IL-4, and IFN.

23 rough the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose function is not complet

24 to control the production of IL-22 in IL-22/IL-17-producing T cells and might thus impact the T-cell

25 synthekine ligands that assembled IL-2Rbeta/IL-4Ralpha or IL-4Ralpha/IFNAR2 receptor heterodimers, t

26 Th1/2 lineage commitment genes (GATA3, IL-4, IL-4R, STAT4 and TBET) in umbilical cord DNA at birth in

27 ase of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymphoid cells (ILC2s

28 suppressing pro-inflammatory interleukin-6 (IL-6) expression after interleukin-1 beta (IL-1beta) sti

29 osis factor alpha (TNF-alpha)/interleukin-6 (IL-6) in infected kidneys.

30 tran gut translocation, serum interleukin-6 (IL-6) levels, bacteremia, and sepsis mortality.

31 lungs, consistent with expression of ESAT-6, IL-6 and phosphorylated-STAT3 in Mtb-infected mouse lung

32 th monocyte chemoattractant protein-1, IL-6, IL-1beta, and is associated with increased MyoD expressi

33 Conversely, abrogating IL-21 receptor signaling in donor T cells and inhibiting

34 inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and activation of p38/Stat pathways

35 e protected from diabetes-induced TNF-alpha, IL-1beta, ICAM-1, and NOS2 upregulation.

36 In vivo alphaCD20-IL-21 therapy resulted in a significant tumor control in

37 While ambient IL-6 was sufficient to suppress the induction of express

38 n of thymic ILCs improved thymopoiesis in an IL-22-dependent fashion.

39 tight-junction protein expression through an IL-10RA-dependent mechanism.

40 and activator of transcription 3 through an IL-23/acutely transforming retrovirus AKT8 in rodent T-c

41 s eosinophilic asthma was associated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL

42 also accompanied by increased Caspase-1 and IL-1beta cleavage upon NLRP3, but not AIM2 or NLRC4 infl

43 MPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.

44 High levels of IL-10 and IL-12/23p40 were significantly associated with amyloid d

45 d increased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

46 In animal models, IL-12 and IL-23 participate in the development of malignant neopla

47 rosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues.

48 observed significant reductions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels

49 tokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

50 Histamine, IL-17, and IL-22 stimulated RANKL expression in RA monocytes and JN

51 the immunomodulatory cytokines IL-1alpha and IL-10 were significantly decreased, and the levels of IL

52 cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in MPs from acute CF

53 , which utilizes the cooperation of IL-2 and IL-33 to enhance Treg- and ILC2-mediated protection from

54 ased tissue produce high levels of CCL-2 and IL-8 and contribute to the inflammatory process promotin

55 MATERIAL AND IL-22- and IL-17-positive T cells were sorted from human peripheral

56 it is not known whether endogenous IL-4 and IL-13 contribute to the maintenance of peripheral tolera

57 patients is induced by TH2 cells, IL-4, and IL-13 and HDAC activity.

58 In particular, IL-5- and IL-13-producing type 2 ILCs (ILC2s) have been implicated

59 lower frequencies of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th

60 on of the proinflammatory cytokines IL-6 and IL-12p40 while enhancing the release of the regulatory/a

61 hat proinflammatory stimulants LPS, IL-6 and IL-1beta up-regulated the expression of HCA2 on macropha

62 ith Neu5Ac stimulated expression of IL-6 and IL-8 and rescued the tumor growth and migratory phenotyp

63 ar brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in autoreact

64 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in teleost fish.

65 tolerogenic molecules (HLA-G, TGF-beta, and IL-10) were tested on a mixed lymphocyte reaction betwee

66 ted inflammasome activation, cell death, and IL-18 secretion, suggesting that restoring mitophagy and

67 SCFAs inhibited IFN-gamma and IL-17A production in peripheral blood mononuclear cells

68 n and decreased interleukin (IL)-4, IL10 and IL-13 protein levels.

69 ip between TNFAIP3/A20 expression levels and IL-17A production.

70 MATERIAL AND IL-22- and IL-17-positive T cells were sorted from human

71 Ndfip1 restricts Treg cell metabolism and IL-4 production via distinct mechanisms, as IL-4 deficie

72 f MyD88 post-translational modifications and IL-1-driven inflammation.

73 SP (0.01-1 muM) and IL-33 (1-100 ng/mL) in combination also greatly stimulat

74 sion of inflammation-related genes NLRP3 and IL-1beta in Nrf2-deficient kidneys after UUO.

75 yrin IX more efficiently attenuated PGE2 and IL-6 release in HG+IL-1beta-treated cells than in NG+IL-

76 not CFP10 induced STAT3 phosphorylation and IL-6 expression in the mouse lungs, consistent with expr

77 ated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL1RL1) mRNA expression.

78 27 reduced the proinflammatory (TNFalpha and IL-1beta) and increased the anti-inflammatory (IL-10 and

79 in (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble interleukin-6 receptor (sIL-6R).

80 vivo by its naturally occurring antagonist, IL-18 Binding Protein (IL-18BP).

81 l death was prevented with neutralizing anti-IL-2 Ab or STAT5/JAK3 inhibitors, indicating that STAT5

82 IL-4 production via distinct mechanisms, as IL-4 deficiency does not prevent hyperproliferation or e

83 nstead to locally produced cytokines such as IL-33.

84 ion factors and output of cytokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

85 engineered synthekine ligands that assembled IL-2Rbeta/IL-4Ralpha or IL-4Ralpha/IFNAR2 receptor heter

86 nt molecular brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in

87 Here, we focus on a imidazolium based IL and use particle-probe rheology to (i) catch this phe

88 (IL-6) expression after interleukin-1 beta (IL-1beta) stimulation.

89 ion of STAT3 to regulate the balance between IL-12/IL-23 subunits causing a cytokine milieu rich in I

90 We found a significant correlation between IL-34 and TGF-beta1 expressions.

91 le of IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated

92 ells, trans-presentation of IL-6 by DC-bound IL-6Ralpha (called 'IL-6 cluster signaling' here) was ne

93 ether VEGF release by HPMCs is controlled by IL-6 in combination with its soluble receptor (IL-6 tran

94 Acute or chronic stimulation by IL-4 modified expression of more than 1000 genes express

95 second cluster can be rapidly suppressed by IL-10 even after transcription is initiated, and this is

96 tion of IL-6 by DC-bound IL-6Ralpha (called 'IL-6 cluster signaling' here) was needed to prevent prem

97 asthmatic patients is induced by TH2 cells, IL-4, and IL-13 and HDAC activity.

98 ditions of IL-2 deficiency, and, conversely, IL-2 represses Flicr expression.

99 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in

100 of the regulatory/anti-inflammatory cytokine IL-10.

101 ic increase of the pro-inflammatory cytokine IL-1beta.

102 gh brain levels of the inflammatory cytokine IL-1beta.

103 show that LSK(-) cells produce the cytokine IL-17 in response to Plasmodium infection.

104 g release of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymphoid cells

105 those activated by the endogenous cytokines IL-2, IL-4, and IFN.

106 the levels of the immunomodulatory cytokines IL-1alpha and IL-10 were significantly decreased, and th

107 production of the proinflammatory cytokines IL-6 and IL-12p40 while enhancing the release of the reg

108 Moreover, the NLRC3 CARD alone could dampen IL-1beta secretion and ASC speck formation induced by NA

109 We also see evidence of decreased IL-6 pathway signaling in islets from donors with type 2

110 Myoferlin knockdown significantly decreased IL-6-mediated tumor cell migration, tumorsphere formatio

111 This myeloid-derived IL-1beta did not vitally contribute to the generation an

112 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in tel

113 However the role of lipin-2 during IL-1beta production remains elusive.

114 Runx2 was up-regulated by 6.4-fold during IL-13-induced goblet cell differentiation of human bronc

115 However, it is not known whether endogenous IL-4 and IL-13 contribute to the maintenance of peripher

116 In vitro, IL-17A enhanced IL-13-induced gene expression in asthma-relevant murine

117 Exogenous IL-15 exacerbates the severity of sepsis by activating N

118 ses and placental development in DC expanded IL-10(-/-) dams.

119 CD138(+) MPhi expressed IL-10R, CD206, and CCR2 but little TNF-alpha or CX3CR1.

120 Despite being constitutively expressed, IL-18 expression was increased and sustained after stimu

121 Metabolic phenotyping of Foxp3-expressing IL-17A(+), ex-Th17 and iTreg cells demonstrates the diss

122 smokers (OR = 1.99, 95% CI: 1.15, 3.44) for IL-6 and among former smokers (OR = 2.83, 95% CI: 1.18,

123 smokers (OR = 1.30, 95% CI: 0.69, 2.44) for IL-8.

124 -specific CD4 T cells were then analyzed for IL-13 and IFN-gamma expression.

125 -) ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice

126 f the IL-12A gene (IL12A), which encodes for IL-12p35, have been associated with pSS.

127 These follicles were strongly positive for IL-15, which was primarily presented in its membrane-bou

128 tantly, the uptake of exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted react

129 utput of cytokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

130 of inflammatory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), and attenuated the wast

131 elated with lower frequencies of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expre

132 ns of Th1/2 lineage commitment genes (GATA3, IL-4, IL-4R, STAT4 and TBET) in umbilical cord DNA at bi

133 cant downregulation of Th17-associated genes IL-17A, IL-22, and retinoic acid-related orphan receptor

134 Global IL-6 inhibition in the early phase after fracture reduce

135 tingly, Th22 cells also expressed granzymes, IL-13, and increased levels of Tbet.

136 ently attenuated PGE2 and IL-6 release in HG+IL-1beta-treated cells than in NG+IL-1beta-treated cells

137 n numbers and frequency but expressed higher IL-4 levels than those from nonatopic subjects.

138 Histamine, IL-17, and IL-22 stimulated RANKL expression in RA monoc

139 udy forms a strong basis for using humanized IL-27 toward the treatment of post-menopausal osteoporos

140 t signals through the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose function is

141 PLCgamma/PKC-induced mTOR activation impairs IL-7-mediated B cell development.

142 k loop to control the production of IL-22 in IL-22/IL-17-producing T cells and might thus impact the

143 , iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondrocytes.

144 Furthermore, changes in IL-6 following stress predicted intraindividual variabil

145 rified Wogonin mimicked the effects of F4 in IL-1beta-stimulated OA chondrocytes.

146 NA sequencing to reveal the heterogeneity in IL-4-induced I transcription.

147 In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with ca

148 IL-1alpha was directly involved in IL-8 production and likely contributed to neutrophilic a

149 larger skin lesions and satellite lesions in IL-1R1(-/-) mice.

150 3 subunits causing a cytokine milieu rich in IL-23 to favour Th2 polarization.

151 y, a critical analysis of speeds of sound in ILs vs those in classical molecular solvents is presente

152 e suppression of catabolic markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in

153 release of inflammatory molecules, including IL-1beta.

154 Increased IL-1beta boosts local antimicrobial peptides to facilita

155 es to promote viral clearance, but increased IL-22 in vivo decreased T cell numbers and functions in

156 c urticaria which is associated by increased IL-31 serum levels.

157 P-deficient monocytes demonstrated increased IL-6, increased nitrite, and decreased bacterial replica

158 ell as boosting the ability of LPS to induce IL-1beta mRNA and pro-IL-1beta while inhibiting the prod

159 vely, these studies suggest that LPS-induced IL-10 promotes the down-regulation of MC surface Fcepsil

160 rotein kinase A pathway is potently inducing IL-1beta transcription, as well as boosting the ability

161 M. tuberculosis-infected IL-21R KO mice had enhanced bacterial burden and reduced

162 ecreased the production of anti-inflammatory IL-10, and stimulated the secretion of IL-6.

163 -1beta) and increased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

164 sis showed that PRN694 effectively inhibited IL-17A production from murine T helper type 17-different

165 PGE2 We showed previously that PGE2 inhibits IL-27 production in murine bone marrow-derived DCs.

166 ta T cells provide an early source of innate IL-17, which promotes antimicrobial peptide production,

167 Interleukin (IL)-13 is a pleiotropic T helper type 2 cytokine frequen

168 vel of proinflammatory cytokine interleukin (IL)-12 correlates with the severity of periodontitis.

169 0 mRNA expression and decreased interleukin (IL)-4, IL10 and IL-13 protein levels.

170 OX treatment not only increases interleukin (IL)-33 released from breast tumor cells, which is crucia

171 Levels of interleukin (IL)-13 in BAL were also significantly decreased after an

172 Increased expression of Interleukin (IL)-33 has been detected in intestinal samples of patien

173 ed tumor necrosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues.

174 with a type 2 immune response (interleukin [IL]5 gene, IL13, and IL13RA2) and a type 17 immune respo

175 ially, some differences in biomarker levels (IL-1beta and sRANKL) and bacterial species between peri-

176 findings identify a novel mechanism linking IL-6 trans-signaling and angiogenesis in the peritoneal

177 poration of different kinds of ionic liquid (IL) can increase the electrode sensing current toward di

178 Ionic liquids (ILs) have recently been developed as a novel class of lu

179 BOP, less increase in GCF volume, and lower IL-1beta total amount/concentration.

180 e found that proinflammatory stimulants LPS, IL-6 and IL-1beta up-regulated the expression of HCA2 on

181 e conclude that ESAT-6 stimulates macrophage IL-6 production through STAT3 activation.

182 promote proliferation and induce or maintain IL-22 production by ILC3s and determine a molecular mech

183 y act as the bridging molecule that mediates IL-37 binding to the TGF-beta receptor complex.

184 In animal models, IL-12 and IL-23 participate in the development of malign

185 at express the Tr1-cell-associated molecules IL-10, inducible T-Cell costimulator (ICOS), lymphocyte

186 mat than those of WKY rats and produced more IL-17F on induction.

187 ith B. pertussis produced significantly more IL-17 than gammadelta T cells from infected unprimed mic

188 Moreover, IL-22 deficiency enhanced T cell responses to promote vi

189 Moreover, IL-33 increases NK-1 gene and surface protein expression

190 s independent of IL-26, because both natural IL-26 released by Th17 clones and rhIL-26 lacked antimic

191 ease in HG+IL-1beta-treated cells than in NG+IL-1beta-treated cells.

192 signaling and Treg differentiation, but not IL-2 expression.

193 icant reductions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased

194 be important in the development of numerous IL-36gamma-driven pathologies, in addition to psoriasis.

195 ltured for 4 d in the presence or absence of IL-4.

196 Absence of IL-4Ralpha limits thymocyte emigration, leading to an in

197 mechanistic insights into the activation of IL-36gamma and highlight that cathepsin S-mediated activ

198 ight that cathepsin S-mediated activation of IL-36gamma may be important in the development of numero

199 delta, but IL1RAPL1 mediates the activity of IL-1beta on dendrite morphology.

200 mportant questions about how the assembly of IL-12 family members is regulated and controlled in the

201 tory monocytes and pharmacologic blockade of IL-1beta or NLRP3 abrogated this phenotype.

202 licr is particularly marked in conditions of IL-2 deficiency, and, conversely, IL-2 represses Flicr e

203 cytokine, which utilizes the cooperation of IL-2 and IL-33 to enhance Treg- and ILC2-mediated protec

204 nhanced by priming with physiologic doses of IL-5.

205 The effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene

206 chanisms behind the pro-angiogenic effect of IL-37 are less well understood.

207 tle is known regarding the direct effects of IL-4 on keratinocyte function.

208 atment in mice led to sustained expansion of IL-33 receptor-positive kidney ILC2s and ameliorated adr

209 Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pa

210 medium with Neu5Ac stimulated expression of IL-6 and IL-8 and rescued the tumor growth and migratory

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

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

213 Loss and gain of IL-10RA expression directly correlates with IEC barrier

214 0 surface proteins enabled identification of IL-4-upregulated surface proteins, such as CD90, CD108,

215 Our findings underscore the importance of IL-10R signaling in preventing T-cell- and cytokine-medi

216 is antimicrobial activity was independent of IL-26, because both natural IL-26 released by Th17 clone

217 but it also participates in the induction of IL-13 receptors and miR-126a expressed on/in the MDSCs.

218 cells, which is crucial for the induction of IL-13(+) Th2 cells, but it also participates in the indu

219 TGF-beta1 and BMP-2 as potent inhibitors of IL-34 expression in RA synovial fibroblasts.

220 In contrast, the kidneys of IL-36 receptor (IL-36R) knockout mice exhibit attenuated

221 High levels of IL-10 and IL-12/23p40 were significantly associated with

222 thogenic T cells that produce high levels of IL-17 in response to IL-23.

223 murine macrophages produce reduced levels of IL-18 and are unable to optimally stimulate IFN-gamma pr

224 e significantly decreased, and the levels of IL-2 in the serum of AOM rats increased after KJT treatm

225 tion was assessed by using in vivo models of IL-13-induced lung pathology and in vitro culture of mur

226 spondyloarthritis, and increased numbers of IL-17A(+)GM-CSF(+) double-producing CD4, CD8, gammadelta

227 ctor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Ralpha (called 'IL-6 cluster signal

228 4 T cells exhibit an increased production of IL-17A, an effect that is accompanied by an increased si

229 In this article we show high production of IL-1beta in biopsy samples and Leishmania antigen-stimul

230 e feedback loop to control the production of IL-22 in IL-22/IL-17-producing T cells and might thus im

231 trophils, along with increased production of IL-5, prostaglandin D2, and eosinophil and T-helper type

232 We observed significant reductions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-

233 o known as PTPN2, as a negative regulator of IL-7R-STAT signaling in T cell progenitors, contributing

234 e through several steps including release of IL-33, which promotes cytokine (IL-5, IL-13) production

235 The functional role of IL-27 and CD301b(+) cells is demonstrated by the finding

236 To confirm a possible modulatory role of IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL

237 atory IL-10, and stimulated the secretion of IL-6.

238 ta support a model wherein a pre-TfH wave of IL-4 secreted by interfollicular NKT cells triggers the

239 The effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene expressio

240 the effect of endogenously produced PGE2 on IL-1beta production.

241 ents at the time of clinical presentation on IL-10 production and its association with S. aureus bact

242 gands that assembled IL-2Rbeta/IL-4Ralpha or IL-4Ralpha/IFNAR2 receptor heterodimers, that do not occ

243 Knockdown of GP130 or IL-2Rgamma induced cell death in selected JAK inhibitor-

244 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in teleost fish.

245 In particular, IL-5- and IL-13-producing type 2 ILCs (ILC2s) have been

246 17 cytokine-mediated signaling, particularly IL-17C.

247 Peripheral IL-1 inhibition using anakinra for 4 weeks does not resu

248 ility of LPS to induce IL-1beta mRNA and pro-IL-1beta while inhibiting the production of TNF-alpha.

249 activation, which mediates synthesis of pro-IL-1beta during inflammasome priming.

250 ted with overt production of proinflammatory IL-1beta.

251 rogression is conditional on proinflammatory IL-1 genetic variations.

252 occurring antagonist, IL-18 Binding Protein (IL-18BP).

253 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in MPs from

254 In contrast, the kidneys of IL-36 receptor (IL-36R) knockout mice exhibit attenuated TILs after UUO.

255 -6 in combination with its soluble receptor (IL-6 trans-signaling).

256 ts infected with L. braziliensis and reduced IL-1beta levels after cure.

257 of transcription 3 phosphorylation, reduced IL-2 production, and enhanced activation and survival.

258 ttle is known about mechanisms that restrain IL-17 cytokine-mediated signaling, particularly IL-17C.

259 em and PCs after a boost with rLBNSE, rLBNSE-IL-7-immunized mice promptly produced a more potent seco

260 ted with neutrophilic asthma and with sputum IL-1beta protein levels, whereas eosinophilic asthma was

261 -1 and P2X7 receptor activation to stimulate IL-1beta release.

262 To study IL-17-related cytokines in nasal/bronchial biopsies from

263 Tristetraprolin suppresses IL-27 production by promoting p28 mRNA degradation.

264 Short-term IL-33 treatment in mice led to sustained expansion of IL

265 ysregulated production of GM-CSF rather than IL-17 induces spontaneous immunopathology in a mouse mod

266 ction factors, it was intuitive to find that IL-34-Mphis possess significantly greater mRNA levels of

267 We therefore hypothesized that IL-15(-/-) mice will have reduced inflammatory responses

268 Here, we report that IL-15(-/-) mice developed enhanced allergic responses in

269 The result suggests that IL-37 induces pro-angiogenic responses through TGF-beta,

270 The IL acts as a neutral base catalyst in which the contact

271 The IL-1beta-induced formation of NEMO-containing structures

272 The IL-23-mediated effects are accompanied by an increase in

273 investigate the role of neutrophils and the IL-17A pathway in mediating pediatric severe therapy-res

274 Furthermore, the IL-10 expressing NK cells markedly enhanced angiogenic r

275 IL-19, a member of the IL-10 cytokine family that signals through the IL-20 rec

276 Likewise, polymorphisms of the IL-12A gene (IL12A), which encodes for IL-12p35, have be

277 By solving the crystal structure of the IL-1alpha/aptamer, we provide a high-resolution structur

278 ale mice exhibited greater expression of the IL-4Ralpha and estrogen receptor (ER) alpha compared wit

279 ully treated with therapeutics targeting the IL-1 pathway; however, there are a number of identified

280 In this article, we show that the IL-33-induced cytokine production is only partly depende

281 -10 cytokine family that signals through the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cyt

282 vate STAT3 signalling in hepatocytes through IL-6 produced in the liver microenvironment.

283 Thus, IL-22-induced claudin-2 upregulation drives diarrhea and

284 or primary human epithelial cells exposed to IL-13, IL-17A, or both.

285 The mechanisms leading to IL-10 expression by CD4(+) T cells are being elucidated,

286 patients who show only a partial response to IL-1 blockade.

287 iRNAs (isomiRs) to the miRISC in response to IL-1beta, including miR-146a-5p, miR-155-5p and miR-27b-

288 produce high levels of IL-17 in response to IL-23.

289 he role of Act1 in keratinocyte responses to IL-17 using a tetracycline inducible short hairpin RNA t

290 n with S. aureus conferred responsiveness to IL-20 that manifested as modification of actin polymeriz

291 erferon-independent mechanism involving Toll-IL-1-receptor domain-containing adapter-inducing IFN-alp

292 e in vivo, which could be rescued by topical IL-27 treatment.

293 Unlike IL-1beta, which inhibits B lymphopoiesis by acting on ea

294 Specifically, we used IL-23 in vivo gene transfer to induce arthritis in mice

295 In vitro, IL-17A enhanced IL-13-induced gene expression in asthma-

296 these findings suggest a new paradigm where IL-4-dependent up-regulation of Cox-1 expression may pla

297 d IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased in peripheral blood of clini

298 rt the "To Go or To Grow" hypothesis whereby IL-13Ralpha2 serves as a molecular switch from invasion

299 es, resulting in a TH17 immune response with IL-23 as a key driver.

300 ys and, in particular, by supplementing with IL-12.