ライフサイエンスコーパス: IL-23

1 IL-23 (interleukin 23) regulates immune responses agains

2 IL-23 activates the synthesis and production of leukotri

3 IL-23 has been well studied in the context of T cell dif

4 IL-23 inhibition attenuated disease by decreasing coloni

5 IL-23 is a key driver of pathogenic Th17 cell responses.

6 IL-23 is associated with plaque psoriasis susceptibility

7 IL-23 is instrumental in expanding extrathymically gener

8 IL-23 is significantly increased in infected mice with a

9 IL-23 mediates expansion of T helper 17 (Th17) cells, wh

10 IL-23 orchestrates exclusion of adaptive T and B cells a

11 IL-23 was found to be essential for melanocyte homeostas

12 IL-23, a cytokine highly expressed in psoriatic skin les

13 IL-23, composed of the cytokine subunit p19 and the solu

14 IL-23, in turn, promoted the expression of IL-17A in bot

15 IL-23-elicited osteoclastogenesis is independent of the

16 IL-23-mediated induction of psoriasis is reduced in AQP3

17 the pathway such as interleukin-12 (IL-12), IL-23, IL-17A, and IL-17RA have variably beneficial effe

18 ng tumor necrosis factor (TNF), IL-6, IL-12, IL-23, and IL-1beta.

19 Combining IL-12/IL-23 blockade and acitretin may constitute an efficient

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

21 r, as a consequence of the inverted IL-12p70/IL-23 ratio following beta2AR stimulation, LPS-stimulate

22 ecretion, leading to a shift in the IL-12p70/IL-23 ratio.

23 qPCR analysis revealed IL-10, IL-12, IL-13, IL-23 and TGFbeta were elevated, these were not statisti

24 g cytokines IL-12p70, IFNgamma, IL-5, IL-13, IL-23, and IL-6 production in vivo.

25 kade of the interleukin 23-helper T cell 17 (IL-23-TH17) pathway with ustekinumab represents an effic

26 nflammatory Th17 cytokines, including IL-17, IL-23, and IL-1beta, impaired blood-brain barrier integr

27 odontal disease pathogenesis regarding IL-17/IL-23 axis, with a decreasing effect on ABL and gingival

28 is to determine levels of IL-1beta, IL-17A, IL-23, and lipopolysaccharide (LPS) in saliva, and to ex

29 es, such as IL-1beta, IL-12, IL-17A, IL-17F, IL-23, and tumor necrosis factor (TNF); chemokine recept

30 from non-pregnant, females secrete IL-1beta, IL-23 and IL-6 and stimulate T cells to produce IL-17a u

31 were due to an autocrine effect of IL-1beta/IL-23-mediated induction of IL-6 production in alpha1KO

32 mma, TNF-alpha, IL-2, IL-17A, IL-17F, IL-22, IL-23, and IL-1beta) and decreased levels of anti-inflam

33 kin 12p70 and an increase in interleukin 23 (IL-23) production by gp120-treated mDCs.

34 Expression of interleukin 23 (IL-23), IL-1 receptor I (IL-1RI), IL-17R, tissue inhibit

35 Interleukin-23 (IL-23) and IL-17 are cytokines currently being targeted

36 Interleukin-23 (IL-23) is a pro-inflammatory cytokine required for the p

37 Interleukin-23 (IL-23) is considered a critical regulator of IL-17 in ly

38 Interleukin-23 (IL-23), an IL-12 family cytokine, plays pivotal roles in

39 as crucial effectors of the interleukin-23 (IL-23)-granulocyte macrophage colony-stimulating factor

40 t assay: 1) IL-1beta; 2) IL-6; 3) IL-17A; 4) IL-23; and 5) transforming growth factor- beta.

41 the presence of IL-6 and TGF-beta (or IL-6, IL-23, and IL-1beta) resulted in increased numbers of IL

42 ominant asthma had increased IL-1beta, IL-6, IL-23, C3a, and serum amyloid A levels in BAL fluid, and

43 mal lymphopoietin, and periostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P < .05).

44 ody briakinumab and by leveraging additional IL-23:antibody complexes, we propose a mechanistic parad

45 of phosphorylated STAT3 within 30 min after IL-23 stimulation.

46 deficiency also conferred resistance against IL-23-induced psoriasis.

47 ibrary with the cellular activity against an IL-23-stimulated transcriptional response in T lymphocyt

48 act IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine.

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

50 pDCs are the primary sensors, leading to an IL-23/TH17 deviation.

51 nd growth factors, including IL-6, IL-11 and IL-23 as well as CCL2, CCL5, CXCL7, CXCL5, ICAM1 and TGF

52 as consisting of pro-inflammatory IL-12 and IL-23 and the anti-inflammatory IL-27 and IL-35 cytokine

53 interleukin (IL)-12-type cytokines IL-12 and IL-23 are involved in T-helper (Th) 1 and Th17 immunity,

54 DED-induced IL-12 and IL-23 are required for in vivo transition of pathogenic

55 effective for treating psoriasis, IL-12 and IL-23 p40 inhibition attenuates Crohn's disease, whereas

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

57 based on the documented role that IL-12 and IL-23 play in autoimmune diseases through differentiatin

58 ted by CB1, able to promote either IL-12 and IL-23 release from keratinocytes or TH1 and TH17 polariz

59 IL-12 and IL-23 responses were analyzed at the transcriptional and

60 Stimulation with IL-12 and IL-23 results in activation of receptor-associated Janus

61 Although cytokines, such as IL-12 and IL-23, have been shown to shape plasticity of ILCs, litt

62 H1- and TH17-polarizing cytokines, IL-12 and IL-23, respectively.

63 in (IL)-12/23p40 subunit shared by IL-12 and IL-23.

64 the protein subunit common to both IL-12 and IL-23.

65 mmatory cytokines interleukin 12 (IL-12) and IL-23 connect innate responses and adaptive immune respo

66 nd interleukin (IL)-1beta, IL-10, IL-12, and IL-23 expression and secretion were quantified by flow c

67 nonfunctional box motifs abolish IL-12- and IL-23-induced STAT3 phosphorylation and cytokine-depende

68 IL-12 family members IL-12p70 and IL-23 are important for host immunity against Candida sp

69 s by differential regulation of IL-12p70 and IL-23 cytokine subunits.

70 m of differential regulation of IL-12p70 and IL-23.

71 and enhanced IL-6, TNF-alpha, IL-12p70, and IL-23 production following TLR4 ligation.

72 significant differences in plasma IL-17 and IL-23 between patients with keratitis and uninfected ind

73 with monoclonal antibodies against IL-17 and IL-23 has shown considerable promise.

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

75 d salivary levels of interleukin (IL)-17 and IL-23.

76 trix metalloproteinase 9 (MMP-9), IL-17, and IL-23 release from infiltrated inflammatory cells.

77 evation and reduction profiles of IL-17A and IL-23 are detected in saliva of patients with LP and GP.

78 s found between concentrations of IL-17A and IL-23 or IL-1beta.

79 Salivary concentrations of IL-17A and IL-23 were elevated significantly in patients with LP co

80 levated levels of IFN-gamma, IL-17alpha, and IL-23, as well as increased accumulation of Ag-specific

81 elated with increased levels of IL-1beta and IL-23 mRNA.

82 nnate immune signaling, because IL-1beta and IL-23 stimulate T cell subsets producing IL-22, another

83 We demonstrate that IL-1beta and IL-23 together are able to promote the development of bo

84 particularly in the presence of IL-1beta and IL-23.

85 that are stable in the presence of IL-2 and IL-23.

86 ounterregulation between the TSLP/type 2 and IL-23/type 17 axes.

87 L-17A(+), IL-17F(+), IL-21(+), IL-22(+), and IL-23(+) cells were examined by immunohistochemistry in

88 tion of interleukin 17A (IL-17A), IL-22, and IL-23 in the tongue after infection, as well as for the

89 vity-related upregulation of serum IL-23 and IL-23 receptor in patients with systemic lupus erythemat

90 c also leads to lower levels of IL-23p19 and IL-23 and higher levels of IL-12p35.

91 L-12p70 levels were higher, and IL-23p19 and IL-23 levels were lower in both SAM11-treated mice and B

92 nificantly increased expression of IL-33 and IL-23, cytokines that promote ILC2 and ILC3, respectivel

93 on via ILC-extrinsic regulation of IL-33 and IL-23.

94 on of interleukin 1beta (IL-1beta), IL-6 and IL-23 and anti-fungal responses of the TH17 subset of he

95 IL-23, and between plasma IL-17 and IL-6 and IL-23.

96 uroinflammatory diseases, including IL-6 and IL-23.

97 s induced the release of IL-1beta, IL-6, and IL-23 by DCs, but addition of these cytokines or superna

98 ased PD-L1 and decreased IL-1beta, IL-6, and IL-23 expression, as well as a reduced capacity to drive

99 17-instructing cytokines IL-1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell differentiation was

100 ines, such as TNF-alpha, IL-1beta, IL-6, and IL-23.

101 observed an increase in numbers of IL-6- and IL-23-producing dendritic cells in OVA-exposed Ptx3(-/-)

102 rough an aryl hydrocarbon receptor (AhR) and IL-23 receptor pathway.

103 ption-dependent mechanisms for TNF-alpha and IL-23 and posttranscriptional mechanisms for caspase-1-d

104 Cytokines IL-1beta, IL-6, TGF-beta1, and IL-23 were the only requirement for the development of b

105 Co-blockade of both CCL9 and IL-23 abrogates Myc-induced tumor progression.

106 thelial-derived signaling molecules CCL9 and IL-23 as the principal instructing signals for stromal r

107 n response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A-independent actions.

108 Il12b; collectively called 'Il12' here) and IL-23 (Il23a and Il12b; collectively called 'Il23' here)

109 the activation of the NLRP3 inflammasome and IL-23/IL-17 axis.

110 against various immune axes (TH2, TH22, and IL-23/TH17).

111 e of IL-1 signaling suppresses both TSLP and IL-23 expression and ameliorates skin inflammation.

112 n by thymic stromal lymphopoietin (TSLP) and IL-23, respectively.

113 ng affinity for an anti-interleukin-23 (anti-IL-23) antibody by using the complementary approaches of

114 ng of and signaling blockade by the 7B7 anti-IL-23 antibody.

115 onsideration of anti-TH2, anti-TH1, and anti-IL-23 targeting strategies.

116 geted therapeutics has cemented psoriasis as IL-23/TH17 polarized.

117 This dichotomy between IL-23 and IL-17 was effectively modeled in the multidrug

118 A link between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling

119 how that M1 increase NK cell cytotoxicity by IL-23 and IFN-beta-dependent upregulation of NKG2D, IL-1

120 ologies after activation of T lymphocytes by IL-23.

121 insights into receptor complexes mediated by IL-23, and by IL-12 family members in general, have rema

122 colonic CD103(+) CD11b(-) DC is repressed by IL-23.

123 -1R1-deficient T cells was fully restored by IL-23 polarization and expansion in vitro Therefore, our

124 data define a novel pathway that is used by IL-23 in myeloid cells and identify a major mechanism fo

125 IL-12-polarized Th1 cells, IL-23-polarized Th17 cells, and Th17 cells that acquire

126 3/p19 did, however, not act as a competitive IL-23 antagonist but, at higher concentrations, induced

127 When added in SLE T cell in vitro cultures, IL-23 induced IL-17 and limited IL-2 production, whereas

128 he induction of the proinflammatory cytokine IL-23 in macrophage-like cells.

129 Discovery of the cytokine IL-23, which shares a common p40 subunit with IL-12, pro

130 a levels of IL-22 and its upstream cytokine, IL-23, are highly elevated in patients after major liver

131 RORgammat-deficient mice showed decreased IL-23-induced psoriasis-like skin inflammation and cytok

132 DC-derived IL-23 is known to act on CD4(+) T cells to induce IL-22

133 hage-derived or CD103(-) CD11b(+) DC-derived IL-23 is required to negatively control the otherwise de

134 the Delta9 mRNA and consequently diminishes IL-23 signaling.

135 However, the mechanisms that drive IL-23 production by skin DCs in response to cutaneous se

136 ress IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD

137 l structure capable of binding to endogenous IL-23.

138 ption factor T-bet is required to facilitate IL-23-driven pathogenic effector functions; however, the

139 as second receptor for IL-12 and IL-23R for IL-23 signal transduction.

140 show that site II of p19 is dispensable for IL-23 signaling.

141 lexes, we propose a mechanistic paradigm for IL-23 and IL-12 whereby cognate receptor binding to the

142 ere psoriasis, supporting a central role for IL-23 in psoriasis pathogenesis.

143 RORgammat and increased mRNA transcripts for IL-23 receptor (IL-23R) and IL-26, demonstrating inflamm

144 Furthermore, IL-23 modulated the cutaneous microenvironment by limiti

145 Furthermore, IL-23 was also elevated in THP(-/-) kidneys.

146 immunity and related pathology, we generated IL-23 receptor-deficient MRL.lpr mice.

147 tantly, proteolytically released sIL-23R has IL-23 binding activity.

148 tains 20 non-silent mutations, cleaves human IL-23 at the target peptide bond, and when pre-mixed wit

149 sequence, HPLVGHM, that is present in human IL-23.

150 We determined a crystal structure of human IL-23 in complex with its cognate receptor, IL-23R, and

151 -based aptamer, highly specific to the human IL-23 cytokine, with picomolar activity.

152 growth of keratinocytes both ex vivo and in IL-23-injected ears of mice.

153 of chronic inflammation and tissue damage in IL-23-mediated immune diseases and it suggests the GM-CS

154 At week 4, significant decreases in IL-23/TH17 pathways were observed that persisted through

155 iasiform skin inflammation with increases in IL-23 and IL-17A and proinflammatory monocytosis and neu

156 mmat modulator with therapeutic potential in IL-23/IL-17 mediated autoimmune diseases.

157 rence has been associated with reductions in IL-23-induced IL-17A production and STAT3 phosphorylatio

158 3 subunits causing a cytokine milieu rich in IL-23 to favour Th2 polarization.

159 The Th17 network, including IL-23 and IL-22, has recently emerged as a critical comp

160 macrophages, as a major source of increased IL-23 synthesis.

161 ibe psoriatic Mo-MDSC that produce increased IL-23, IL-1b, and CCL4 cytokines compared to Mo-MDSC fro

162 gp120-induced IL-23 upregulated suppressor of cytokine signaling 1 (SO

163 mary cultures of murine splenocytes inhibits IL-23-mediated immune signaling.

164 the skin changes induced either by injecting IL-23 or by application of the TLR7 agonist imiquimod.

165 Vdelta1 T cells by a mechanism that involves IL-23 release by DCs.

166 ranscription factor Blimp-1 (Prdm1) as a key IL-23-induced factor that drove the inflammatory functio

167 IL-23R (sIL-23R) variants, which might limit IL-23-mediated immune responses.

168 proinflammatory M1 type phenotype (IL-10(low)IL-23/IL-1beta/IL-6(high)), and these M1 Mvarphi showed

169 The M5 IL-23 mutant differs from wild-type by five alanine subs

170 LMO4 appears to mediate IL-23-related responses in psoriatic keratinocytes and i

171 The TH17-associated mediators IL-23 and macrophage inflammatory protein 3alpha/CCL20 w

172 Furthermore, we observed IL-23-induced SOCS1 binding to the IFN-gamma transcripti

173 as an animal model of MS) in the absence of IL-23 and IL-12, respectively.

174 Specifically, the absence of IL-23 expression in macrophages or CD11b(+) DC results i

175 ng protective IL-17 intact in the absence of IL-23.

176 A direct action of IL-23 on primary melanocytes, shown to be IL-23R(+), dem

177 help to explain why p40 is an antagonist of IL-23 and IL-12 signaling and show that site II of p19 i

178 Instead, binding of IL-23 to the cytokine binding module of IL-12Rbeta1 is m

179 Furthermore, blockade of IL-23 leads to reduced mortality in the context of macro

180 To examine whether targeted blockade of IL-23 or IL-17A in KC-Tie2 psoriasis mice improves cardi

181 We propose that blockade of IL-23 should have a therapeutic value in patients with S

182 ther, these data address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 ce

183 Furthermore, deficiency of IL-23, which was diminished in IL-36R knockout UUO mice,

184 essential transcription factor downstream of IL-23 that acts in concert with RORgammat to activate th

185 Increased frequencies of IL-23(+) APCs in the colon were found post-PBio treatmen

186 kin-23/-17 axis led to the identification of IL-23 and IL-17 as important participants in the pathoge

187 Our data show that targeted inhibition of IL-23 or IL-17A improves psoriasis-like skin disease and

188 vidence suggests that specific inhibition of IL-23 would result in improvement in psoriasis.

189 mouse skin induced by the local injection of IL-23.

190 e I and III paradigm but that interaction of IL-23 to IL-12Rbeta1 is independent of site II in p19.

191 structural insights from the interaction of IL-23 with the inhibitory antibody briakinumab and by le

192 ficantly different among groups was level of IL-23 (P <0.05).

193 LPDCs produced high levels of IL-23, IL-6 and TGFbeta when stimulated with commensal f

194 and IL-22 did not involve the modulation of IL-23 but rather PGE2; PGE2 was significantly increased

195 study identifies T-bet as a key modulator of IL-23-driven colitogenic responses in the intestine and

196 gammadelta T cells which, in the presence of IL-23 and IL-1beta, produce large quantities of interleu

197 In the presence of IL-23, IL-22 production is independent of aryl hydrocarb

198 ive pathways in the skin drive production of IL-23 by CD301b(+) dDCs resulting in IL-17A production f

199 We analyzed the production of IL-23 in vitro by blood and skin DCs.

200 and Jnk1/2, and augmented the production of IL-23.

201 In this paper, we describe a novel role of IL-23 in myeloid cell differentiation.

202 17 differentiation, particularly the role of IL-23 in promoting the differentiation of a pathogenic s

203 To further dissect the role of IL-23 in the expression of autoimmunity and related path

204 This study unveiled the role of IL-23-dependent IL-17 induction in LdCen(-/-) parasite-i

205 tion, emerging evidence supports the role of IL-23-driven Th17 cells in inflammation.

206 Secretion of IL-23, IL-1, and TNF-alpha, the cytokines required for t

207 ate the inflammatory process by secretion of IL-23.

208 restructured the helical IL-23p19 subunit of IL-23 and restrained its IL-12p40 subunit to cooperative

209 IL12B transcripts, which encode subunits of IL-23, a macrophage cytokine that stimulates production

210 In light of the beneficial targeting of IL-23/12 in patients with IBD, 1,25D appears as an inter

211 uble positive thymocytes and upregulation of IL-23 by dendritic cells.

212 an IL-22 response, supporting the utility of IL-23 and IL-22 blockade in AD.

213 xpression by tape stripping was dependent on IL-23 and gammadelta T cells.

214 Th17 cell maturation depends on IL-23 signaling.

215 Five peptide regions on IL-23 with reduced backbone amide solvent accessibility

216 udy, we assessed the requirement of IL-12 or IL-23 stimulation, as well as Th plasticity, for the dif

217 nd produced IL-10 and CCL18 but not IL-12 or IL-23.

218 of p40 than p40 homodimer (p402), IL-12, or IL-23.

219 recombinant CXCL1 and CXCL5 but not IL-17 or IL-23 plus IL-1beta rescued bacterial burden in the etha

220 Moreover, disruption of IL-33 or IL-23 signaling attenuated cytokine-producing ILC2 and I

221 k2 with IL-23R is mandatory for IL-12 and/or IL-23 signaling, whereas Tyk2 seems to be dispensable.

222 lly, we have identified that in human PBMCs, IL-23 induces the expression of MDL-1, a PU.1 transcript

223 ntage IL-17 producing neutrophils and plasma IL-23, and between plasma IL-17 and IL-6 and IL-23.

224 lls become polyfunctional upon IL-1beta plus IL-23 stimulation, cosecreting IL-17A, IL-17F, IL-22, GM

225 ation of nociceptors, DDCs failed to produce IL-23 in imiquimod-exposed skin.

226 soriasis induced by imiquimod or recombinant IL-23 injection when challenged as adults, with increase

227 Treatment with recombinant IL-23, which is required for stabilization and maintenan

228 of IL-10, and the addition of IL-10 reduces IL-23 production by intestinal macrophages.

229 cells and resistance to C. albicans required IL-23 production from CD301b(+) dermal dendritic cells (

230 s associated with severe asthma and requires IL-23 receptor (IL-23R) signaling, which is negatively r

231 t DNA repair of damaged melanocytes requires IL-23.

232 Serum IL-23 levels were higher in groups 1 and 2 than groups 3

233 sease activity-related upregulation of serum IL-23 and IL-23 receptor in patients with systemic lupus

234 es a significant portion of the steady-state IL-23/IL-22 axis.

235 lerization of dendritic cells by suppressing IL-23 production.

236 roles in intestinal immunity, and targeting IL-23/12 is a promising approach in IBD therapy.

237 Whereas antibodies targeting IL-23 ameliorate colitis, IL-17 neutralization exacerbat

238 reated with each of the antibodies targeting IL-23, IL-17A, or IL-17RA, consistent with clinical effi

239 cularly psoriasis, where biologics targeting IL-23 and IL-17 have shown significant clinical efficacy

240 ta associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting cons

241 el-related AD responses, with increased TH17/IL-23 skewing.

242 Our data associate a shared TH17/IL-23 immune fingerprint with the major orphan forms of

243 se, with additional activation of TH22, TH17/IL-23, and TH1 cytokine pathways depending on the subtyp

244 n mechanically injured skin and caution that IL-23 and IL-22 blockade in patients with AD may enhance

245 We demonstrate that IL-23 released by keratinocytes in response to endogenou

246 Our data challenge the dogma that IL-23 and Th17 plasticity are universally required for t

247 Moreover, we find that IL-23-induced inflammation requires expression of CCR6 b

248 Our results show that IL-23 accounts for the main aspects of human and murine

249 We also show that IL-23 is released in human skin after scratching and pol

250 whereas IL-23R-blocking studies showed that IL-23 was required for optimal C. albicans-induced IL-17

251 irulent Leishmania challenge suggesting that IL-23 plays an essential role in IL-17-mediated protecti

252 The IL-23 receptor (IL-23R) complex consists of the unique I

253 The IL-23-driven tissue-resident group 3 innate lymphoid cel

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

255 The IL-23/IL-17 pathway is implicated in autoimmune diseases

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

257 ries were constructed and panned against the IL-23 target, resulting in a single-digit muM hit and su

258 , the coordinate expression of CD11c and the IL-23 receptor defines an IL-10-regulated, colitogenic m

259 53 ameliorated skin inflammation in both the IL-23-induced ear swelling model and the topical imiquim

260 L-22 in the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target

261 6 is a fully human IgG1 mAb specific for the IL-23 p19 subunit.

262 IL-36gamma is important for the IL-23/IL-17-dominated inflammation and anti-BCG Th1 immu

263 The discovery of the central role for the IL-23/type 17 T-cell axis in the development of psoriasi

264 eresting therapeutic agent that inhibits the IL-23 receptor pathway, providing a novel mechanism for

265 L-17f, and IL-22; topical application of the IL-23 aptamer decreased both IL-17f and IL-22 by approxi

266 inds to a receptor complex consisting of the IL-23 receptor (IL-23R) and the IL-12 receptor beta1 (IL

267 esponded to 1,25D with downregulation of the IL-23 receptor pathway.

268 ion of signal transduction downstream of the IL-23 receptor represents an intriguing approach to the

269 on and strongly attenuated expression of the IL-23 receptor, IL-17, and GM-CSF.

270 n critically depended on coexpression of the IL-23 receptor, which was required for maximal inflammat

271 Components of the IL-23 signaling pathway, such as IL-23R, JAK2 and STAT3,

272 lls but modifies qualitative features of the IL-23-driven colitogenic response by negatively regulati

273 In this case report, a role of the IL-23-TH17-axis in PRP was identified, suggesting a shar

274 , we propose a non-canonical topology of the IL-23.IL-23R.IL-12Rbeta1 complex.

275 ulates proximal epithelial activation of the IL-23/IL-17 axis and systemic neutrophilia.

276 findings reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production an

277 consequences of inhibiting components of the IL-23/T-helper cell 17 pathway-the target of next-genera

278 onlesional levels; and (3) inhibition of the IL-23/TH17 pathway.

279 kin bacteria are engaged in induction of the IL-23/type 17 axis.

280 eration of drugs that selectively target the IL-23/Type 17 T cell axis.

281 eport provides a rationale for targeting the IL-23-TH17-pathway as a treatment option for refractory

282 ne diseases, particularly those in which the IL-23/IL-17 axis has been implicated, has risen in the l

283 Among them, IL-23 is essential for the generation of stable and ence

284 unladen macrophages expressed high TNFalpha, IL-23 & iNOS and lower IL-10 & CD163.

285 essed high IL-10 & CD163 and lower TNFalpha, IL-23 & iNOS irrespective of macroscopic inflammation.

286 r, IL-23R, and revealed that IL-23R bound to IL-23 exclusively via its N-terminal immunoglobulin doma

287 but did not result in significant changes to IL-23 mRNA levels, confirming that the aptamer did not g

288 nctional responses of human mucosal ILC3s to IL-23 plus IL-1beta stimulation.

289 phabeta and gammadeltaT cells in response to IL-23, the role of T cells and IL-23 has overshadowed an

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

291 biophysical properties similar to wild-type IL-23 (monomeric state, thermal stability, and secondary

292 ave no measurable differences from wild-type IL-23 except for binding of and signaling blockade by th

293 the ability to develop a Th17 phenotype upon IL-23 stimulation.

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

295 In vitro IL-23 treatment promoted IL-17 production and downregula

296 ve IL-17A, and this production of IL-17A was IL-23 independent, leaving protective IL-17 intact in th

297 ssion of lesional skin genes associated with IL-23/IL-17 signaling pathways and normalization of psor

298 target peptide bond, and when pre-mixed with IL-23 in primary cultures of murine splenocytes inhibits

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

300 ILC3s stimulated with IL-23 plus IL-1beta upregulated the vitamin D receptor a