ライフサイエンスコーパス: IL-17

1 IL-17 can act directly on neurons to alter their respons

2 IL-17 deficiency can be bypassed by optogenetic stimulat

3 IL-17 expression correlates with expression of GM-CSF by

4 IL-17 induced MMP7 and EMT in human prostate cancer LNCa

5 IL-17 is a cytokine known primarily for its role in infl

6 IL-17 is a pro-inflammatory cytokine implicated a variet

7 IL-17 is rapidly produced during lung injury and signifi

8 IL-17 promotes prostate adenocarcinoma with a concurrent

9 IL-17 receptor C and Pten double KO mice recapitulated t

10 IL-17-induced NOTCH1 activation results in the interacti

11 IL-17-producing gammadelta T (gammadeltaT-17) cells have

12 IL-17-producing gammadelta T (gammadeltaT17) cells are c

13 IL-17-related cytokines expression was amplified in bron

14 atriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, malondialdehyde, and fetuin-a.

15 ed TH2 and TH17 responses, including IL-13(+)IL-17(+)CD4(+) double-producing effector T cells.

16 nflammatory cytokines including IL-4, IL-13, IL-17 and TNF-alpha.

17 actor-alpha, epidermal growth factor, IL-13, IL-17, IL-1alpha, and inducible protein-10.

18 e tested the hypothesis that interleukin 17 (IL-17) and tumor necrosis factor (TNF) are key cytokines

19 mmatory phenotype, producing interleukin 17 (IL-17) and/or interferon gamma (IFN-gamma).

20 ghtened interferon gamma and interleukin 17 (IL-17) production as well as by high levels of T-bet and

21 ), as well as an increase of interleukin 17 (IL-17) production by intestinal cells.

22 erferon-gamma (IFN-gamma) or interleukin 17 (IL-17), but the role of the T cell antigen receptor (TCR

23 Interleukin-17 (IL-17) and IL-17 receptor (IL-17R) signaling are essenti

24 he proinflammatory cytokines interleukin-17 (IL-17) and interferon-gamma (IFNgamma) in multiple model

25 The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involve

26 Interleukin-17 (IL-17) is a critical pro-inflammatory cytokine, which ha

27 Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates

28 ction, including the role of interleukin-17 (IL-17), which is important in controlling other fungal i

29 or alpha (TNF-alpha) but not interleukin-17 (IL-17).

30 coexpression of IFN-gamma, TNF-alpha, IL-2, IL-17, and/or IL-22 in CD4 T cells and IFN-gamma-express

31 g the KD025 inhibits the secretion of IL-21, IL-17, and interferon gamma along with decreasing phosph

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

33 known about the functions of miRNAs in IL-22/IL-17-producing T cells.

34 tivation of the NLRP3 inflammasome and IL-23/IL-17 axis.

35 odulator with therapeutic potential in IL-23/IL-17 mediated autoimmune diseases.

36 The IL-23/IL-17 pathway is important in multiple autoimmune diseas

37 atients and enhanced the production of IL-4, IL-17, and TGF-beta1 by these lymphocytes in contrast to

38 kines (TNF-alpha, IL-1beta, IFN-gamma, IL-6, IL-17) and accumulation of activated macrophages were si

39 ation of interleukin (IL)-1beta, IL-4, IL-6, IL-17, and tumor necrosis factor-alpha using an assay sy

40 Histamine, IL-6, IL-17, IL-21 and IL-22 induced the expression of H4R in

41 Plasma interleukin (IL) 2, IL-4, IL-5, IL-7, IL-17, interferon-gamma, and tumor necrosis factor-alpha

42 involves matrix metalloproteinase 9 (MMP-9), IL-17, and IL-23 release from infiltrated inflammatory c

43 of gamma interferon (IFN-gamma), IL-5, IL-9, IL-17, and IL-22 and decreased production of IL-10 follo

44 was used to measure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T cells.

45 h22 polar cytokines (i.e. IL-5, IL-13, IL-9, IL-17, IL-22).

46 Over-activating IL-17 receptors abnormally heightens responses to 21% ox

47 the absence of gamma/delta T cells or after IL-17 neutralization, this epithelial response was drama

48 Clinical trial data for mAbs against IL-17 signaling (secukinumab, ixekizumab, and brodalumab

49 Alongside IL-17 induction, we observed induction of IFN-gamma-prod

50 tionately higher among Th17 cells than among IL-17(-) or gamma interferon-positive (IFN-gamma(+)) cel

51 ng unbiased genetic screens, we delineate an IL-17 signalling pathway and show that it acts in the RM

52 in response to S. aureus PSMalpha drives an IL-17-mediated skin inflammatory response to epicutaneou

53 ratinocyte differentiation and results in an IL-17-linked psoriasis-like skin inflammation.

54 In psoriasis, an IL-17-mediated inflammatory skin disease, skin lesions r

55 sing prior to transplant, confirming that an IL-17-sensitive gut microbiota controls susceptibility t

56 related with IL-17A (r = 0.74, P < .001) and IL-17/TNF-synergistic/additive gene expression.

57 f new therapeutic targets in IFN-, IL-1- and IL-17-mediated diseases.

58 elper cytokines of either disease, IL-13 and IL-17.

59 by increased pSTAT3, IL-4, IL-5, IL-13, and IL-17, and % CD4(+) T cells that produce IL-5, IL-13, an

60 CD4(+) T cells that produce IL-5, IL-13, and IL-17.

61 Interleukin-17 (IL-17) and IL-17 receptor (IL-17R) signaling are essential for regu

62 lls were sources of IFN-gamma and IL-17, and IL-17-producing cells expressed RORgammat.

63 ry cytokines TNF-alpha, IFN-gamma, IL-2, and IL-17.

64 ersed the Abeta-induced changes in IL-22 and IL-17 and the ratio of Bax/Bcl-2.

65 Importantly, while both IL-22 and IL-17 mediate skin GVHD, Th17-induced chronic GVHD can b

66 IL-22 and IL-17, Bax and Bcl-2, PKA/PKG and the brain derived neur

67 hest expression for miR-323-3p in IL-22- and IL-17-double-positive T cells and its capacity to suppre

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

69 IL-22- and IL-17-producing T cells have important roles in allergic

70 ta T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation.

71 HDM inhalation also increased serum IL-4 and IL-17 levels and increased BALF % CD4(+) T cells that pr

72 gammat and production of IFN-gamma, IL-4 and IL-17, respectively.

73 ially produce cytokines IFN-gamma, IL-4, and IL-17, respectively, upon activation.

74 amma interferon (IFN-gamma), IL-4, IL-5, and IL-17 production by lung lymphocytes in immunocompetent

75 s were associated with elevation of IL-6 and IL-17, which are important inflammatory cytokines in pul

76 ture but display strong STAT3 activation and IL-17 expression in cocultures with SEA-responsive nonma

77 he sum of T-cell infiltration/activation and IL-17-mediated epidermal responses, was not higher in se

78 nflammatory cytokines, such as TNF-alpha and IL-17.

79 ophils and secretion of IL-6, TNF-alpha, and IL-17 in contrast to the eosinophilic inflammation and I

80 lammatory markers (IFN-gamma, TNF-alpha, and IL-17) in mice with dextran sodium sulfate-induced colit

81 or the first time implicated CaMKIIalpha and IL-17 as critical regulators of persistent pain in EAE,

82 Increased hepatic Th17 cells and IL-17 expression were observed in NASH mice and patients

83 cell differentiation from naive T cells and IL-17 production in established Th17 cells.

84 e, miR-466i functioned to mediate GM-CSF and IL-17 mRNA decay, which was confirmed by in vitro lucife

85 ession of T helper cell type-2 cytokines and IL-17, associated with a reduced ability to maintain int

86 e inflammatory responses mediated by DCs and IL-17-producing TCRgammadelta(+) and CD4(+) Th17 T cells

87 secreting cells were most abundant early and IL-17-secreting cells late.

88 ch are defective in RORgammat expression and IL-17 production.

89 Combined treatment with FGF2 and IL-17 synergistically induced ERK activation as well as

90 The production of both IFN-gamma and IL-17 by pulmonary lymphocytes increased during infectio

91 2- to 3-fold higher levels of IFN-gamma and IL-17 in peripheral blood mononuclear cells compared wit

92 iR-24 drives the production of IFN-gamma and IL-17 in T cells at least in part through targeting TCF1

93 have reduced proliferation and IFN-gamma and IL-17 production.

94 CD8(+) T cells were sources of IFN-gamma and IL-17, and IL-17-producing cells expressed RORgammat.

95 Production of both IFN-gamma and IL-17, in response to AChR, was also restricted to the C

96 crease in IL-4 and decrease in IFN-gamma and IL-17-expressing CD4(+) T cells were observed in DMF-tre

97 nied by reduced frequencies of IFN-gamma and IL-17-producing CD4(+) cells and induction of antiinflam

98 IFN-gamma and IL-17-producing cells specific for the hemagglutinin and

99 m which is dependent on interferon gamma and IL-17.

100 led to reduced frequencies of IFN-gamma- and IL-17-expressing cells, indicating that ROS play a role

101 severe disease, the numbers of IFNgamma- and IL-17-producing CD4 T cells infiltrating the CNS tissues

102 xpression could be upregulated by itself and IL-17 in inflammatory cells.

103 ession modulation, even considering PAR2 and IL-17, which has not been investigated thus far.

104 ypothesis that enhanced TH17 programming and IL-17 expression in abundant CD161(+) immune cells in SH

105 n 11c (CD11c)/diphtheria toxin receptor, and IL-17 receptor A(-/-) mice were used to examine T-lympho

106 ain and neuropathy in multiple sclerosis and IL-17 may act upstream of CaMKIIalpha in the generation

107 cell-mediated enhancement; conversely, anti-IL-17, but not anti-IL-13, attenuated the enhancement by

108 eleased IL-1alpha and IL-36alpha, as well as IL-17 production by gammadelta T cells and ILC3 and neut

109 t and survival by oral epithelial cells, but IL-17 also stimulated them to express IL-36gamma.

110 The cytokine IL-22 is often coproduced by IL-17-secreting cells.

111 o the skin inflammation, which was driven by IL-17-producing gammadelta and CD4(+) T cells via direct

112 genes or markers synergistically induced by IL-17 and TNF-alpha (IL-17A/C, IL-19, CXCL1, PI3, CCL20,

113 nes involved in host defense were induced by IL-17 in a TRAF3IP2-dependent fashion.

114 the extent of infiltration of CD45(+) CD4(+) IL-17(+) cells, CD45(+) CD34(+) collagen I(+) CXCR4(+) f

115 ages of CD3(+)CD4(+)IL-13(+) and CD3(+)CD4(+)IL-17(+) cells in MLNs and decreased Il13 and Il17a and

116 ion toward increased proinflammatory CD3+CD4+IL-17+ and reduced tolerogenic Foxp3+ Treg lymphocytes (

117 ing moderate-to-severe psoriasis, confirming IL-17 as an important driver of this disease.

118 r induction of the pro-inflammatory cytokine IL-17.

119 Significantly, the Th17 cytokine IL-17 not only stimulated the expression of important re

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

121 er local increases in inflammatory cytokine (IL-17) production, which could have important enteric he

122 1, T cell polarization resulted in decreased IL-17(+) and increased Foxp3(+) cells during both in vit

123 They decreased IL-17-producing cells and increased the level of circula

124 s study unveiled the role of IL-23-dependent IL-17 induction in LdCen(-/-) parasite-induced immunity

125 nflammation involving IL-36R/MyD88-dependent IL-17 T cell responses.

126 hus, the transcriptional circuitry directing IL-17 expression inhibits cytotoxic functions.

127 how that the transcription factors directing IL-17 production, STAT3 and RORgammat, inhibit cytotoxic

128 Disrupting IL-17 signalling reduces RMG responsiveness to input fro

129 peptides was reduced in the absence of early IL-17.

130 to abrogated cytotoxic function and ectopic IL-17 production in CD8(+) T cells.

131 Neutralization of either IL-17 or IFN-gamma abrogated LdCen(-/-) -induced host pr

132 allogeneic T cells and in the use of either IL-17/arginase I or IFN-gamma/inducible nitric oxide syn

133 Thus, diabetes-enhanced IL-17 alters the oral microbiota and renders it more pat

134 elB-deficient CD4(+) T cells showed enhanced IL-17 induction and exacerbated the disease.

135 suppressed, whereas its inhibition enhanced, IL-17-driven inflammation in keratinocytes.

136 ith BA, cholangiocytes were found to express IL-17 receptor A, and the prevalence of IL-17A(+) cells

137 tory Th17 cells, or their ability to express IL-17.

138 s key roles for TNF and, to a lesser extent, IL-17 as mediators of liver inflammation and fibrosis in

139 ere, we report a pathogenic role of the FGF2-IL-17 cooperation in the pathogenesis of autoimmune arth

140 nockout mice, deficient in the receptors for IL-17 (IL-17RA) and interferon (IFN)-gamma (IFNgammaRI),

141 cipient germ-free mice, oral microbiota from IL-17-treated donors induced reduced neutrophil recruitm

142 show that human peripheral blood IFN-gamma(+)IL-17(+) (TH1/17) and IFN-gamma(-)IL-17(+) (TH17) CD4(+)

143 IFN-gamma(+)IL-17(+) and IFN-gamma(-)IL-17(+) subsets constituted se

144 FN-gamma(+)IL-17(+) (TH1/17) and IFN-gamma(-)IL-17(+) (TH17) CD4(+) T cells display distinct transcri

145 IFN-gamma(+)IL-17(+) and IFN-gamma(-)IL-17(+) subsets constituted secondary TH types, and BAL

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

147 ell effector cytokines, including IFN-gamma, IL-17, and IL-21.

148 ponse effect on the production of IFN-gamma, IL-17, IL-10, and IL-13, with reductions observed at hig

149 regs, and decreased the levels of IFN-gamma, IL-17, IL-6, and TNF-alpha.

150 In this study, we show that the gut IL-17-producing gamma/delta T (gamma/delta T17) cells de

151 The absence of IL-2 also resulted in higher IL-17 production and the emergence of IL-17(+)IFN-gamma(

152 s and observed that PA strains induce higher IL-17 levels than PH strains.

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

154 CD14+ monocytes were treated with histamine, IL-17, IL-21 and IL-22, and a H4R antagonist (JNJ7777120

155 n myeloid derived cells in mice deficient in IL-17 or TNF.

156 Despite the increases in IL-17 production during infection, IL-17A-deficient mice

157 of psoriasis-related genes and reduction in IL-17 gene expression.

158 as accompanied by a significant reduction in IL-17(+) cells in the draining lymph nodes.

159 esting that IL-23 plays an essential role in IL-17-mediated protection by LdCen(-/-) parasites.

160 of DN T cells, decreased IL-2, and increased IL-17 production.

161 during H. pylori infection led to increased IL-17-mediated responses and increased neutrophil accumu

162 genesis through induction of EMT, indicating IL-17-MMP7-EMT axis as a potential target for developing

163 SLE T cell in vitro cultures, IL-23 induced IL-17 and limited IL-2 production, whereas T follicular

164 In vitro exogenous IL-6-induced IL-17 production in iTreg cells, and in vivo conversion

165 Inducing IL-17 expression in adults can rescue mutant defects wit

166 interfering RNA knockdown of MMP7 inhibited IL-17-induced EMT.

167 ting the IL-17RA-NOTCH1 interaction inhibits IL-17-induced NOTCH1 activation and attenuates Th17-medi

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

169 n certain autoimmune diseases through innate IL-17 production.

170 Intestinal IL-17-producing cells, including Th17, gamma/delta T, an

171 ated orphan receptor gammat or intracellular IL-17 was not affected.

172 se seemingly variegated processes by keeping IL-17 receptor signaling in check while supporting diffe

173 independently of the IL-22(+) Th17 lineage, IL-17 signaling to donor Th22 directly promotes their de

174 ore likely to maintain their ability to make IL-17, were more potent proinflammatory cytokine produce

175 Whether MMP7 mediates IL-17's action and the underlying mechanisms remain unkn

176 hese findings demonstrate that MMP7 mediates IL-17's function in promoting prostate carcinogenesis th

177 ed gammadeltaT-17 cells was able to moderate IL-17 and affect differentiation into polyfunctional cyt

178 ne a crucial role for miR-146a in modulating IL-17-driven inflammation in the skin.

179 bial protein calprotectin without modulating IL-17 expression.

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

181 mAbs that neutralize IL-17 or its receptor have proven efficacious in treatin

182 Neutralizing Ab to IFN-gamma, but not IL-17, inhibited nevus development (p < 0.01).

183 ng genetic background in which activation of IL-17 signaling is central in the pathogenesis.

184 Intratracheal administration of IL-17 provoked a neutrophilic response in the airways of

185 eased amounts of IL-2 and reduced amounts of IL-17 compared with T cells from wild type animals.

186 dritic cells 2 produced increased amounts of IL-17 with concomitant heightened epithelial antimicrobi

187 Microarray analysis of IL-17 family cytokines was performed in H. pylori-infect

188 lungs of CD8(-/-) recipients were capable of IL-17 production and expressed high levels of signature

189 We saw remarkable concordance of IL-17-controlled gene expression in C. albicans-infected

190 Strikingly, temporal control of IL-17-producing gammadeltaT (gammadeltaT17) cell differe

191 reases IL-1beta, and promotes development of IL-17-dependent, Th cell-transferable protective immunit

192 is supported by the fact that disruption of IL-17 signaling (IL-17 receptor A(-/-)) prevented airway

193 phages, as well as systemic dysregulation of IL-17 and IFN-gamma responses.

194 Elimination of IL-17 reduced sialadenitis more drastically in females t

195 higher IL-17 production and the emergence of IL-17(+)IFN-gamma(+) double producers.

196 which these regulators control expression of IL-17-dependent inflammatory genes, as well as the major

197 n inflammation, with increased expression of IL-17-induced keratinocyte-derived inflammatory mediator

198 ed CNS inflammation and reduced frequency of IL-17- and GM-CSF-producing CD4(+) T cells.

199 survival, expansion and effector function of IL-17-producing helper T (T(H)17) cells during autoimmun

200 we propose novel collaborative functions of IL-17 and IFN-gamma, acting through neutrophils and macr

201 of Tbx21 has no effect on the generation of IL-17/IFN-gamma double-producing cells, but leads to a m

202 There was also induction of IL-17 and its promoting cytokines in total splenocytes a

203 The striking induction of IL-17-related genes or markers synergistically induced b

204 ocular inflammation via the infiltration of IL-17-producing gammadeltaT-cells, which are presumably

205 ss both the activators and the inhibitors of IL-17 signal transduction, and also the physiological im

206 mechanism contributes to the instability of IL-17-producing T cells.

207 gammadelta T cells and heightened levels of IL-17 and IL-36 family of cytokines starting 1 week afte

208 f ABL was conducted and expression levels of IL-17 and RORgammat in gingival tissues were evaluated i

209 ammatory macrophages, and elevated levels of IL-17 and TNF.

210 The expression levels of IL-17 are correlated with a number of essential clinical

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

212 Our data showed that despite their loss of IL-17 expression, ex-Th17 cells were more polyfunctional

213 Loss of IL-17-producing cells in the gut during HIV infection is

214 equired for stabilization and maintenance of IL-17, heightened Th17, and Tc17 responses in immunized

215 Using a preclinical model of IL-17-mediated dry eye disease, we demonstrate that upon

216 The neutralization of IL-17 prior to infection significantly improved the outc

217 ated MC specifically increased the number of IL-17-producing T cells.

218 man CD4(+) and CD8(+) T cells and numbers of IL-17-producing CD4(+) mouse splenocytes, respectively.

219 s of ichthyosis and raise the possibility of IL-17-targeting strategies.

220 lenic stromal cells grown in the presence of IL-17 enhanced the production of CXCL12, a chemokine ass

221 n pancreas, and down-regulated production of IL-17 and IFN-gamma in CD4(+) and CD8(+) T cells in sple

222 o Notably, B cells altered the production of IL-17, IL-13, and IFN-gamma, supporting a role for B cel

223 While the proinflammatory properties of IL-17 are key to its host-protective capacity, unrestrai

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

225 findings reveal a non-immunological role of IL-17 modulating circuit function and behaviour.

226 didiasis underscore the preponderant role of IL-17 receptor A (IL-17RA) in preserving mucocutaneous i

227 17 cells, appears to be a dominant source of IL-17 in experimental psoriasis.

228 ve proved to be an important early source of IL-17 in many inflammatory settings and are emerging as

229 e that PCs, not ECs, are the major target of IL-17 within the microvessel wall and that IL-17-activat

230 The activation and upregulation of IL-17 in prepsoriatic skin produces a "feed forward" inf

231 the lymph nodes (LNs) that was dependent on IL-17-induced prostaglandin activity.

232 B. pertussis specific and secreted IL-17 or IL-17 and IFN-gamma.

233 ylori-associated diseases, the role of other IL-17 cytokine family members remains unclear.

234 nistration significantly downregulated PAR2, IL-17, TNF-alpha, and IL-1beta mRNA expressions (P <0.05

235 /-) Upon challenge with wild-type parasites, IL-17 and its differentiating cytokines were significant

236 pression of FGF2 in mouse joints potentiated IL-17-induced inflammatory cytokine and chemokine produc

237 Furthermore, the A2AR agonist prevented IL-17 production by murine and human iNKT cells after ac

238 rsus 3.1) and reduced circulating NT-proBNP, IL-17, TNF-alpha, and IL-6 post-treatment (P<0.05).

239 become ex-Th17 cells that no longer produce IL-17 but produce IFN-gamma.

240 et of effector CD8(+) T cells (Tc17) produce IL-17 and fail to express cytotoxic genes.

241 precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually o

242 4(+) T cells and gammadelta T cells produced IL-17.

243 minantly Vgamma4(-)gamma1(-) cells, produced IL-17 in the lungs as early as 2 h after infection.

244 ungs of infected but not naive mice produced IL-17 in response to heat-killed B. pertussis in the pre

245 Th17 cells (CD4(+) T helper cells producing IL-17).

246 consistently higher than for cells producing IL-17, with peak levels of approximately 25 to 30% of CD

247 ung, including activation of proinflammatory IL-17-producing gammadelta T cells, without affecting vi

248 ges and in turn to propagate proinflammatory IL-17 signaling.

249 In vitro IL-23 treatment promoted IL-17 production and downregulated IL-2 production.

250 cally, we found that Neu5Gc exposure reduced IL-17(+) T-cell numbers and supported differentiation of

251 s at H3K9 sites, and consequently repressing IL-17 expression.

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

253 ells were B. pertussis specific and secreted IL-17 or IL-17 and IFN-gamma.

254 ts lacking the ability to generate or signal IL-17 develop intestinal hyper-acute GVHD.

255 both the BCR and a secondary T cell signal, IL-17 can enhance B cell proliferation and germinal cent

256 the fact that disruption of IL-17 signaling (IL-17 receptor A(-/-)) prevented airway neutrophilia in

257 CNV resulted in an increase in splenic IL-17-producing gammadeltaT- and Th17-cells; yet in the

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

259 In summary, IL-17-producing alphabeta T cell clones with psoriasis-s

260 tions for therapeutic strategies that target IL-17, because these may not inhibit pathogenic ex-Th17

261 body-induced arthritis (CAIA), via targeting IL-17 secreting Th17 cells and regulatory T cells (Treg)

262 RORgammat) is a master regulator of the Th17/IL-17 pathway that plays crucial roles in the pathogenes

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

264 f IL-17 within the microvessel wall and that IL-17-activated PCs can modulate neutrophil functions wi

265 Nature, Chen et al. (2017) demonstrate that IL-17 plays a neuromodulatory role in Caenorhabditis ele

266 We further demonstrated that IL-17 contributes to persistent pain in EAE and function

267 There is evidence that IL-17 plays a role in the defense against tuberculosis.

268 We found that IL-17 is responsible for inducing but not maintaining me

269 Here we report that IL-17 stimulation induces NOTCH1 activation in OPCs, con

270 Here we show that IL-17 has neuromodulator-like properties in Caenorhabdit

271 Because previous studies showed that IL-17 plays a protective role during infection with muco

272 the outcomes in the CF mice, suggesting that IL-17 may be a therapeutic target.

273 The IL-17 family cytokines IL-17A and IL-17C drive the patho

274 Accordingly, the IL-17-IL-17R axis may provide an attractive target for t

275 s demonstrate critical crosstalk between the IL-17 and NOTCH1 pathway, regulating Th17-induced inflam

276 h ubiquitin ligase activity that couples the IL-17 receptor to downstream signaling pathways.

277 imethylation and hence further modifying the IL-17 locus for optimal transcription.

278 ke receptor 4 (TLR4) and inactivation of the IL-17 axis resulted in altered immune responsiveness and

279 However, the role of the IL-17 family in genetic hypertension in the spontaneousl

280 rom septic human neonates, expression of the IL-17 receptor emerged as a critical regulatory node.

281 transcription factor that forms part of the IL-17 signaling pathway.

282 interaction of IL-17A and/or IL-17F with the IL-17 receptor A/C (IL-17RA/C).

283 ays postconfluence) markedly amplified these IL-17 responses and increased basal levels and TRAF3IP2

284 a subset of gammadelta T cells committed to IL-17 production and are characterized by the expression

285 rocytes, which were found to express Rai, to IL-17.

286 ll as the major target cells that respond to IL-17 signaling.

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

288 f miR-495 and miR-1192 that were specific to IL-17.

289 osis, mesothelial to mesenchymal transition, IL-17 production, and Th17 cell infiltration in response

290 human normal prostates and prostate tumors, IL-17 mRNA levels were positively correlated with MMP7 m

291 o its host-protective capacity, unrestrained IL-17 signaling is associated with immunopathology, auto

292 ell expression of IL-22 without upregulating IL-17.

293 ion of fetal Vgamma6(+) (but not Vgamma4(+)) IL-17-producing gammadelta T cells and a marked depletio

294 Thus, while IL-17 production in the lungs is increased during Pneumo

295 our study suggests that FGF2 cooperates with IL-17 to promote the pathogenesis of autoimmune arthriti

296 recently reported that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran so

297 of autoimmune arthritis by cooperating with IL-17 to induce inflammatory response.

298 and inhibited in keratinocytes treated with IL-17.

299 Furthermore, treatment with IL-17 antibody decreases the pathogenicity of the oral m

300 ated by naive T cells differentiating within IL-17-secreting T cell and follicular Th cell paradigms