ライフサイエンスコーパス: IL-17

1 IL-17 and IL-17 receptor inhibitors boast an impressive

2 IL-17 antagonists induce impressive clinical benefits in

3 IL-17 family cytokines are critical to host defense resp

4 IL-17 is a highly versatile pro-inflammatory cytokine cr

5 IL-17 mediates immune protection from fungi and bacteria

6 IL-17 produced by T(H)17 cells plays a central role in n

7 IL-17 receptor-A antagonism caused extensive improvement

8 IL-17, a potent proinflammatory cytokine, has been shown

9 IL-17-dependent gene expression, including keratinocyte

10 IL-17-induced elevated intracellular copper level leads

11 IL-17-producing RORgammat+ gammadelta T cells (gammadelt

12 IL-17-producing Th17 cells are implicated in the pathoge

13 nd induce FoxP3(neg) tumor-promoting IL-10(+)IL-17(+)IFNgamma(+ )regulatory CD4(+) T cells.

14 induced by this nematode, TNF-alpha, IL-10, IL-17, IFN-gamma and expressing of FoxP3(+) T cells were

15 rleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17, interferon-gamma and differential T and B cell su

16 was used to measure IFN-gamma, IL-9, IL-13, IL-17, and IL-22 cytokine levels in CD4(+)/CD8(+) T cell

17 IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL11, G-CSF, GM-CSF and

18 ly more interleukin 1beta (IL-1beta), IL-13, IL-17, IL-22, and KC, and showed severe immune cell infi

19 tokines specifically responsible for T(h)17 (IL-17, IL-6, G-CSF) and T(h)1 differentiation and expres

20 show that T-helper 17 (Th17)/interleukin 17 (IL-17)-driven immunity is essential to control oral and

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

22 trate that the production of interleukin-17 (IL-17) during inflammation promotes social behavior in m

23 roles, the ancient cytokine interleukin-17 (IL-17) modulates neural circuit function.

24 ng JAK pathway genes and the interleukin-17 (IL-17) pathway.

25 as to analyze the density of interleukin-17 (IL-17) producing T cells and IL-17 mRNA expression in le

26 On the other hand, interleukin-17 (IL-17) production by Th17 cells increases CDI-associated

27 describe that interleukin-17 (IL-17) re-programs the urea cycle in keratinocytes incre

28 One potential mediator is interleukin-17 (IL-17), a pro-inflammatory cytokine implicated in neurod

29 e readily differentiate into interleukin-17 (IL-17)-producing cells.

30 Interleukin-17 (IL-17)-producing helper T cells (T(H)17 cells) promote i

31 0 (IL-12p40) induction and increased IL-17A (IL-17) production.

32 T cells and dampens the release of IL-1beta, IL-17, and IL-22 in the IMQ-induced model.

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

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

35 ologics that inhibit TNF-alpha, p40IL-12/23, IL-17, and p19IL-23, as well as an oral phosphodiesteras

36 is factor alpha (TNF-alpha), IL-6, IL-12/23, IL-17, IL-4/13, IL-5, immunoglobulin E (IgE), integrins

37 leted or are underway utilizing IL-1, IL-23, IL-17, complement, and Jak inhibition, although there is

38 A dysregulation in the IL-23/IL-17 axis can lead to inflammation of barrier tissues,

39 Activation of the IL-23/IL-17 pathway is integral to the development of psoriasi

40 Dysregulated IL-23/IL-17 responses have been linked to psoriatic arthritis

41 the levels of interleukin (IL)-1beta, IL-6, IL-17, interferon-gamma (IFN-gamma) and superoxide dismu

42 pro-inflammatory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha),

43 els of the cytokines IFN-gamma, IL-13, IL-9, IL-17, and IL-22 in CD4(+)/CD8(+) T cells in the blood o

44 In summary, this study reveals a IL-17-STEAP4-XIAP axis through which the inflammatory re

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

46 pathogenesis, and systemically-administered IL-17 inhibitors are highly effective therapy for modera

47 significant increase of Notch 2, TNF-alpha, IL-17 and RANKL and a significant decrease of Notch 1 an

48 Clinical protocols targeting TNF-alpha, IL-17, and Th17 warrant further testing.

49 Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG) was determined by reverse transcr

50 ng thymic development, but rather acquire an IL-17 bias in the periphery.

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

52 T cells commit to either an IFN-gamma- or an IL-17-producing phenotype through mechanisms that remain

53 m from patients suffering from psoriasis, an IL-17-related disease.

54 se cases amongst psoriasis patients using an IL-17 inhibitor, there remains a lack of evidence to sug

55 ese cells are probably not imprinted with an IL-17 bias during thymic development, but rather acquire

56 28), RANTES (P = .005), IL-2 (P = .002), and IL-17 (P = .007) during viral URIs versus AOMs following

57 ubclinical cows, whereas increased IL-10 and IL-17 gene expression levels were observed for both infe

58 antly reduced the concentration of IL-12 and IL-17 in lymph nodes of treated and contralateral tumors

59 IL-17 and IL-17 receptor inhibitors boast an impressive safety his

60 increased Il17a/interleukin-17A (IL-17A) and IL-17-dependent cytokine expression.

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

62 thelial barrier function, while IL-1beta and IL-17 increase mucin expressions in primary human bronch

63 such as tumour necrosis factor, IL-1beta and IL-17.

64 t is mainly mediated by IL-23, IL-1beta, and IL-17 cytokines.

65 on of CD154, IFN-gamma, TNF-alpha, IL-2, and IL-17 and proliferation.

66 ics that inhibit TNF-alpha, p40IL-12/23, and IL-17 are also approved for the treatment of psoriatic a

67 ity to the human interleukin-23 (IL-23R) and IL-17 receptor A were used.

68 otumoral IL-1alpha, IL-1beta, IL-5, IL-6 and IL-17 and antitumoral IL-2 and IL-12 in tumor-proximal l

69 n NMOSD, elevated IFN-I signatures, IL-6 and IL-17 are associated with severe disability.

70 Furthermore, IL-6 and IL-17 levels are lower in patients on anti-CD20 therapy.

71 ukin-10 (IL-10), IL-12, IL-1alpha, IL-6, and IL-17.

72 y question before us now is whether IL-9 and IL-17 contribute to tumor progression in a sequential an

73 produced by the signatory cytokines IL-9 and IL-17, with gene regulatory profiles evoked by these cyt

74 ccompanied by increased RIPK3 activation and IL-17 production.

75 D-19 with increased Th17 cell activation and IL-17 signaling that may lead to increased likelihood fo

76 ominence of intra-graft memory TNF-alpha and IL-17 double-positive T helper type 17 (Th17) cells is a

77 kin pathology characterized by antiviral and IL-17 immune responses.

78 enhanced response in intracellular Ca2+ and IL-17 expression, which was blocked by SOCE inhibitors 2

79 d sustained influx of Orai1+ CD4 T cells and IL-17 expression was restricted to Orai1+ cells.

80 interleukin-17 (IL-17) producing T cells and IL-17 mRNA expression in lesions representing severe per

81 ks expansion of human gammadelta T cells and IL-17 secretion by human CD4 T cells.

82 s, characterized by decreased diversity, and IL-17/IL-22-related declines in the phylum Firmicutes, c

83 T cell receptor gamma chain expression, and IL-17 production by intestinal gammadelta T cells was ef

84 Production of IFN-gamma and IL-17 from T cells was exacerbated in IL-10 knockout (KO

85 the proinflammatory cytokines IFN-gamma and IL-17 in situ.

86 ereas duration was linked with IFN-gamma and IL-17 levels (P < .04).

87 and systemic M. bovis-specific IFN-gamma and IL-17 production by both gammadelta and CD4 T cells.

88 effector CD8 T cells producing IFN-gamma and IL-17- and IL-4-producing CD4 T cells that cannot mediat

89 CD4 and CD8 T cells producing IFN-gamma and IL-17.

90 perglycemics, IL-1beta, IL-6, INF-gamma, and IL-17 exhibited progressive rewiring.

91 phenotype, effectively induced IFNgamma and IL-17 responses, and failed to orchestrate tissue repair

92 es of mature dendritic cells, IFNgamma-, and IL-17- producing CD4(+)T cells in the dLNs of recipients

93 Topical ACHP also reduced the NF-kappaB and IL-17 inflammatory signature after multiple doses of imi

94 ncreased levels of CXCR2, CXCR2 ligands, and IL-17 receptor within the metastatic lesions.

95 t interaction between the gut microbiome and IL-17/IL-22-producing cells plays a role in the developm

96 mast cells could suppress proliferation and IL-17 and IFN-gamma production by T cells.

97 group, cyclins and cell cycle regulation and IL-17 pathways were likely downregulated, while the same

98 l markers of the Th17 lineage, RORgammat and IL-17, and the Th17 polarisation mediator phospho-STAT3

99 the function of LACC1 in regulating TNF and IL-17 during inflammatory responses.

100 The patient's anti-IL-17 medication was discontinued and endoscopic remissi

101 Furthermore, treatment with anti-IL-17 antibody reduced joint and skin psoriatic arthriti

102 y a clinically relevant dose/schedule of any IL-17-receptor antagonist.

103 wn about IL-17B-F, IL-17A (commonly known as IL-17) has received much attention for its pro-inflammat

104 xis by which inflammatory cytokines, such as IL-17, drive cellular copper uptake via the induction of

105 Moreover, T-bet(-/-) mice have augmented IL-17 and neutrophil numbers, and neutralizing IL-17 red

106 SCs and T cells support tumor growth because IL-17 is tumorigenic in many cancer types and regulatory

107 kpoint in the functional programming of both IL-17- and IFN-gamma-producing gammadelta T cell subsets

108 + T helper 17 (Th17) cells, characterized by IL-17 production, play important roles in the pathogenes

109 cells and immature B cells was increased, by IL-17 deficiency in Roquin(san/san) mice.

110 psoriasis transcriptome and genes induced by IL-17 in keratinocytes were evaluated with microarray pr

111 ially chemoattract peripheral CD27(-) CCR6(+)IL-17 capable of producing gammadelta T cells (gammadelt

112 associated with decreased gammadelta T cell IL-17 and IFN-gamma production in the thymus as well as

113 functionally activated, induce CD4(+) T cell IL-17 expression, and are enriched in the liver of patie

114 ne receptor type 4(+) T helper type 2 cells, IL-17(+) cells, basophils, substance P(+) cells, and der

115 lls, interleukin-(IL)-4-producing Th2 cells, IL-17-producing Th17 cells, follicular T helper (Tfh) ce

116 pemphigus had elevated levels of circulating IL-17(+)(,) T(H)17, T(FH)17, and T(FH)17.1 cells.

117 n entry, they upregulate T-bet and coexpress IL-17, IL-22, and IFN-gamma in a STAT3- and retinoic aci

118 gammadelta T cells that produce the cytokine IL-17 (Tgammadelta17 cells) are innate-like mediators of

119 mice and humans as a source of the cytokine IL-17, which is key for immune resistance to certain pat

120 I-induction of profibrotic T cell cytokines (IL-17, TNF-alpha, IL-9, and IFN-gamma) and chemokine rec

121 ukin (IL)-21, IL-4 and pathogenic cytokines, IL-17 and IFN gamma (IFNy).

122 types that produce the type three cytokines, IL-17 and IL-22.

123 mber, and mucus metaplasia, while decreasing IL-17 mRNA expression.

124 n specifically in beta(2)-integrin-deficient IL-17(+) cells compared to their wild-type counterparts.

125 some evidence that two distinct TCR-defined IL-17-producing gammadelta T cell subsets also exist in

126 ermal cell type, the innate neonatal-derived IL-17 producing gammadelta T (Tgammadelta17) cells, from

127 ogenesis via the direct regulation of dermal IL-17-producing cells and stimulation of keratinocytes f

128 per understanding of the cytokines dictating IL-17 production and the polarity of gammadelta and Th17

129 , SLAMF1 and SLAMF6 expression distinguished IL-17- and IFN-gamma-producing gammadelta T cells, respe

130 equential activation of these factors during IL-17-producing gammadelta T-cell (gammadeltaT17) differ

131 Since the connection of dysregulated IL-17 and psoriasis pathogenesis turned out to be partic

132 suing secretion of pathogenic cytokines (eg, IL-17, interferon-gamma, tissue necrosis factor, granulo

133 rom two Blau syndrome patients show elevated IL-17 and increased CCR7.

134 se CDI-associated mortality through elevated IL-17 production.

135 while permitting T(H)2 cell and, especially, IL-17-producing T helper cell responses, and promoting m

136 Evidently, IL-17-induced release of keratinocyte-derived inflammato

137 requencies of Tc1, CD8(+) T cells expressing IL-17 (Tc17), and CD4(+) T cells expressing IL-17 (Th17)

138 IL-17 (Tc17), and CD4(+) T cells expressing IL-17 (Th17) had shorter durations of hospitalization.Co

139 e we report that 14-3-3zeta is essential for IL-17 signaling by differentially regulating the signal-

140 ded RORgammat+ gammadelta T cells poised for IL-17 production were resistant to C. difficile infectio

141 Investigative Dermatology reveals a role for IL-17 and IFN-gamma, signature cytokines of T-helper 17

142 These studies reveal a role for IL-17 cytokines in mediating CD4-intrinsic immune resist

143 These results reveal an expanded role for IL-17-producing gammadelta T cells in neonatal host defe

144 produce effector cytokines (IL-2, IFN-gamma, IL-17), regardless of differentiation stage.

145 of IL-1R1 and IL-23R and secreted IFN-gamma, IL-17, and GM-CSF in response to canonically restricted

146 ividuals mounted higher levels of IFN-gamma, IL-17, pro-inflammatory cytokines, and IL-10.

147 suring alveolar bone resorption and gingival IL-17 expression as outcomes of Pg-induced inflammation.

148 increase in alveolar bone loss and gingival IL-17 expression over sham-infected animals.

149 d substantially increased numbers of CD44(hi)IL-17(+)IFN-gamma(-) memory T-helper 17 (Th17) cells in

150 High-IL-17 expression was associated with the characteristic

151 cts of IL-17 on cancer biology, focusing how IL-17-mediated inflammatory response and mitogenic signa

152 the ionic environment typical in SLT impairs IL-17 immunity, but the intracellular pathways that medi

153 Murine studies implicate IL-17 and the downstream effects of its inhibition, in t

154 Recent studies implicate IL-17 as a link among inflammation, wound healing, and c

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

156 MO has an unprecedented negative function in IL-17 signaling, distinct from its role in NF-kappaB act

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

158 Guided by recent insights in IL-17 biology, this review aims to explore possible reas

159 vels of proinflammatory cytokines, including IL-17, and increased consumption of the lymphocyte growt

160 on of CD4+ cells from AKI patients increased IL-17, which was blocked by SOCE inhibitors.

161 L-33, and mucous metaplasia while increasing IL-17 expression.

162 Citrobacter rodentium is known to induce IL-17(+) and IL-22(+) CD4(+) T cells (T(h)17 and T(h)22

163 Psoriasis is an inflammatory, IL-17-driven skin disease in which autoantigen-induced C

164 d RV-impeding factors, including interferon, IL-17, and IL-22.

165 ding RORgammat, enabling the conversion into IL-17-producing cells in response to IL-1beta and IL-23.

166 We investigate IL-17 signaling in neurons, and the extent it can alter

167 provide evidence of a link-involving IL-17-between psoriasis and hyperglycemia in humans and

168 with an autoreactive-like profile involving IL-17 and Ccr7.

169 dy participants on the basis of longitudinal IL-17/IL-22 profiles identified discrete groups.

170 ommonly among all ichthyoses, including many IL-17 and TNF-alpha-coregulated genes, which are conside

171 ngs in ASD, suggesting that chronic maternal IL-17 contributes to offspring ASD pathogenesis.

172 or suggests a mechanism for chronic maternal IL-17 effects on offspring.

173 To test chronic maternal IL-17 impacts on offspring, C57BL/6J dams were administe

174 supports a link between the gut microbiome, IL-17/IL-22, and the onset of metabolic diseases.

175 ation, Leukocyte transendothelial migration, IL-17 signaling, Chemokine signaling, C-type lectin rece

176 Moreover, IL-17 increased the expression of CXCR2 ligands and cell

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

178 -17 and neutrophil numbers, and neutralizing IL-17 reduces the neutrophilia but does not affect numbe

179 Postvaccination NKp44(+) and NKp44(+)IL-17(+) ILC frequencies were associated with delayed SI

180 4(+)CCR6(+)T cells expressing IL-10, but not IL-17, were also detectable in the spleens of cytokine r

181 In ovarian cancer (OC), IL-17-producing T cells (Th17s) predict improved surviva

182 nfection showed presymptomatic activation of IL-17- and tumor necrosis factor-related pathways.

183 severe disease had reduced concentrations of IL-17.

184 46 and DASA-58 suppressed the development of IL-17-producing T(H)17 cells but increased the generatio

185 naling complexes that function downstream of IL-17 receptors in C. elegans neurons.

186 lating neural circuit function downstream of IL-17 to remodel physiology and behavior.

187 new understanding of the mitogenic effect of IL-17 on tissue repair and cancer.

188 1 deletion or inhibition blocks expansion of IL-17-secreting gamma4(+)delta4(+) and CD4 T cells and d

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

190 Conversely, abrogating the expression of IL-17 receptor subunit a (IL-17Ra) in the neurons of the

191 sociated with the characteristic features of IL-17-producing gammadelta T (gammadelta17) cells, inclu

192 IL-22, and a tendency to higher fractions of IL-17 producing CD4 + T cells.

193 esembling psoriasis, and high frequencies of IL-17- and IL-22-expressing T cells in blood, correlatin

194 r, it has become clear that the functions of IL-17 are far more nuanced than simply turning on inflam

195 Here, we review the pleotropic impacts of IL-17 on cancer biology, focusing how IL-17-mediated inf

196 IL-10 is only accompanied by an increase of IL-17 in a low IL-2 setting, which is, nevertheless, lik

197 madeltaT cells exacerbate SH, independent of IL-17 expression, by mitigating conventional CD4(+) T-ce

198 Charcot-Leyden crystals, but independent of IL-17.

199 We hypothesized that inhibition of IL-17 would decrease the numbers of T cell subsets that

200 d be substantially reversed by inhibition of IL-17, indicating that host inflammation altered the mic

201 The integration of IL-17 with growth-receptor signaling in specific cell ty

202 ionnaire and immunological investigations of IL-17 responsiveness undertaken.

203 madelta T cells also produced high levels of IL-17 in response to Mycobacterium lipomannan, and deple

204 Higher levels of IL-17 receptor, CXCR2 chemokines, and CXCR2 were observe

205 Individuals distinguished by low levels of IL-17/IL-22 were linked to established markers of metabo

206 seases there is a decline in serum levels of IL-17/IL-22, with concomitant changes in the gut microbi

207 Neutralization of IL-17, but not TNF, prevented enhanced mannan-induced ar

208 displayed a striking increase in numbers of IL-17-producing Vgamma6Vdelta1(+) gammadelta T cells in

209 on and may contribute to the pathogenesis of IL-17-driven inflammatory skin conditions such as psoria

210 Maintenance of a population of IL-17-committed gammadelta T cells in the dermis is impo

211 Here we show an increased presence of IL-17+IL-22+ cells and TGF-beta1 in colorectal cancer co

212 ance, we observed an increased prevalence of IL-17-producing Th17.1 cells in the CSF of HTT gene expa

213 itical for commensal-dependent production of IL-17 and IL-22 by CD4(+) T cells.

214 In addition, males had larger proportions of IL-17 producing T cells than females in both groups.

215 (+) T cells to express an increased ratio of IL-17/IFN-gamma.

216 The role of IL-17 immunity is well established in patients with infl

217 The role of IL-17 in cancer remains controversial.

218 Our aim was to discover the role of IL-17, CXC chemokine receptor 2 (CXCR2) ligands, and can

219 Here, we delve into the dichotomous roles of IL-17 in cancer and provide insight into the tumor micro

220 amma6(+) cells represent the major source of IL-17-producing cells in the gingiva.

221 reprogramming and concomitant suppression of IL-17 cytokine levels and reduced proliferation.

222 cell homeostasis, inhibiting the survival of IL-17-producing Vgamma6Vdelta1(+) cells and promoting th

223 These data support the testing of IL-17/IL-36-targeted therapeutics for patients with icht

224 sed tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing CRC progression.

225 dence suggests that during early oncogenesis IL-17 supports tumor growth, whereas in established tumo

226 To optimize IL-17-based immunotherapy, a deeper understanding of the

227 Accordingly, inhibition of IL-9 or IL-17 cytokines by neutralizing antibodies decreased EMT

228 t, thereby reducing the number of pathogenic IL-17(+)IFN-gamma(+)CD4(+) T cells in the spleen during

229 lated with BAL fungal presence, while plasma IL-17 correlated with BAL fungal presence.

230 ion of an E3-ligase, XIAP, which potentiates IL-17-induced NFkappaB activation and suppresses the cas

231 ous innate and adaptive T cells that produce IL-17 family cytokines have also been described in the h

232 17 cells acquire an inherent bias to produce IL-17 and other "type 17" cytokines during thymic develo

233 the development of Th17 cells, which produce IL-17.

234 Th17 cells (producing IL-17) and Th9 cells (producing IL-9) exhibit functional

235 clerosing cholangitis (PSC) show a prominent IL-17 response upon stimulation with bacteria or fungi,

236 fector function, epithelial RARbeta promoted IL-17 production by intestinal Th17 cells.

237 tective owing to the induction of regulatory IL-17(+)IL-10(+)-coproducing cells.

238 predict that geldanamycin would also revert IL-17-induced goblet cell metaplasia, a prediction confi

239 ke others, we observed induction of a strong IL-17-related gene signature in the vagina during estrog

240 or microenvironment conducive for successful IL-17-based gammadelta and Th17 cell immunotherapy.

241 g) cells were activated by IL-33 to suppress IL-17-producing gammadelta T cells.

242 ary infection, mice deficient in the surface IL-17 receptor B, a component of the IL-25R, exhibited i

243 a number of monoclonal antibodies targeting IL-17 pathways have been approved and are used as first

244 ss the most recent developments in targeting IL-17 for the treatment of chronic inflammation in precl

245 Here, we argue that targeting IL-17 is immunologically plausible as a strategy to prev

246 studies, including clinical trials targeting IL-17.

247 These kinases terminate IL-17 signaling by phosphorylating the adaptor ACT1 lead

248 cell program from follicular T helper (Tfh)-IL-17 to Tfh-IFN-gamma.

249 is essential to promote a population of Tfh-IL-17 cells.

250 Th17/IL-17 and Th9/IL-9 exhibit critical, but often opposing,

251 ata support the emerging consensus that Th17/IL-17 axis signaling is dispensable for the immunopathog

252 standard VVC model masks a role for the Th17/IL-17 axis.

253 are critical for skin homeostasis, and that IL-17 has dual homeostatic and inflammatory function in

254 ing component of IL-17R, we established that IL-17 signaling is regulated by a robust negative feedba

255 Accumulating evidence indicates that IL-17 has important context- and tissue-dependent roles

256 Importantly, we report that IL-17-induced targets of A20 show similar aberrant epide

257 myeloid cells, emerging studies reveal that IL-17 can directly act on tissue stem cells to promote t

258 We further show that IL-17 can directly act on non-Th17 effector CD4+ T cells

259 It is suggested that IL-17 producing T cells represent a significant feature

260 The IL-17 cytokine family comprising IL-17A to IL-17F and re

261 The IL-17 level was increased markedly in Roquin(san/san) mi

262 The IL-17 receptor signaling and specific arms of immunity p

263 The IL-17-high asthma phenotype, characterized by bronchial

264 ed the expression of IL17RA (by 72%) and the IL-17-induced genes IL17C (by 85%), DEFB4 (by 83%), TNFA

265 in unique gammadelta T subsets, such as the IL-17-producing gammadelta T cells.

266 ted directly on myeloma cells expressing the IL-17 receptor to induce a transcriptional landscape tha

267 ritic cells were found to be crucial for the IL-17 signaling pathway and TNF signaling pathway, since

268 gulation of the signal transduction from the IL-17 receptor (IL-17R) remained elusive.

269 attractive targets for immunotherapy in the IL-17 immune axis.

270 vealing a new dimension of complexity in the IL-17 pathway that may help explain its potent and diver

271 However, the role of the IL-17 pathway during VVC remains controversial, with con

272 ct of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC mi

273 We sought to examine the effects of the IL-17 receptor-A antagonist brodalumab, on clinical and

274 ehensive view of the molecular events of the IL-17 signal transduction and its regulation.

275 embers (i.e. IL36RN) but not elements of the IL-17/IL-23 axis.

276 driven IL-10(+) cells, and predominantly the IL-17(+)IL-10(+) double-producing cells, were markedly r

277 ollectively, these data demonstrate that the IL-17-CXCR2 axis facilitates the recruitment of neutroph

278 IL-17D is a cytokine that belongs to the IL-17 family and is conserved in vertebrates and inverte

279 ion of TGFbeta1 in parenchymal cells via the IL-17 receptor C (IL-17RC).

280 Without signaling via the IL-17 receptor, activated FRCs underwent cell cycle arre

281 Therefore, IL-17-producing Th17 cells show promise as a target for

282 In mice, most of these IL-17 producers, termed gammadeltaT-17 cells, actually c

283 Importantly, this IL-17-induced STEAP4-dependent cellular copper uptake is

284 in downstream cytokines IFN gamma, TNFalpha IL-17 and IL-10, hydrocortisone treatment significantly

285 ion disturb the oral microbiota and point to IL-17 as key mediator in this process.

286 tumor growth, whereas in established tumors IL-17 production by gammadelta and Th17 cells potentiate

287 the cytokines IL-12 and IL-13 (ustekinumab), IL-17 (secukinumab, ixekizumab, bimekizumab, and brodalu

288 Origins of vaginal IL-17 in vivo remain unclear, but patient biopsies suppo

289 lates innate gammadelta T-cell responses via IL-17 expression.

290 en Th17 polarisation are intact and in vitro IL-17 responses can be reinvigorated by increasing extra

291 ntiated in the presence of TGF-beta, whereas IL-17-producing effector T cells were additionally expos

292 y expanded, both in blood and liver, whereas IL-17-producing CD4(+) T cells were not.

293 ve provided insights into the means by which IL-17 cooperates functionally with other stimuli in driv

294 While IL-17-mediated production of inflammatory mediators mobi

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

296 ing cells; and T3 CRSsNP was associated with IL-17 signaling, acute inflammatory response, complement

297 rrier measure, significantly correlated with IL-17-regulated gene expression (IL17F and IL36A/IL36B/I

298 enesis and STEAP4 expression correlates with IL-17 level and XIAP activation in human colon cancer.

299 Treating epithelia with IL-17 plus TNFalpha alkalinized ASL pH to ~7.0, increase

300 The patients with IL-17-high asthma were characterized by risk of frequent