ライフサイエンスコーパス: IL-23

1 IL-23 activates the synthesis and production of leukotri

2 IL-23 acts indirectly on Il17ra (+) GC B cells to facili

3 IL-23 and IL-12, two structurally related heterodimeric

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

5 IL-23 contributes to the activation, maintenance, and pr

6 IL-23 depletion with anti-IL-23p19 in vivo also signific

7 IL-23 is a two-subunit cytokine known to promote prolife

8 IL-23 is instrumental in expanding extrathymically gener

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

10 IL-23 promotes autoimmune disease, including Th17 CD4 T

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

14 en completed or are underway utilizing IL-1, IL-23, IL-17, complement, and Jak inhibition, although t

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

16 logy of a group of related cytokines: IL-12, IL-23, and IL-27.

17 On the other hand, IL-12, IL-23, and p40(2) did not exhibit such inhibitory effect

18 erved decrease in p40 and increase in IL-12, IL-23, and p40(2) in serum of mice with experimental aut

19 with a biological role different from IL-12, IL-23, and p40(2) in which it attenuates autoimmune sign

20 pro-inflammatory cytokines including IL-12, IL-23, and type 1 interferons.

21 Importantly, blockade of IL-12, IL-23, or both significantly reduced control of parasite

22 On the other hand, inhibition of IL-12-IL-23, as compared with inhibition of TNF, has greater e

23 Interestingly, p40 arrested IL-12-, IL-23-, or p40(2)-mediated internalization of IL-12Rbeta

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

25 riasis compared with ustekinumab (dual IL-12/IL-23 inhibitor), but comparative molecular effects have

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

27 asing cytokines (eg, interleukin-12 [IL-12], IL-23, IL-6, IL-27, IL-10, transforming growth factor-be

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

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

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

31 Repurposing systemic T helper type 17/IL-23-inhibitory therapies for psoriasis may prove usefu

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

33 n HFD had elevated serum levels of IL-1beta, IL-23, interferon (IFN)-beta, IFN-gamma, monocyte chemoa

34 olecule showed excellent activity in an IL-2/IL-23-induced mouse pharmacodynamic study and demonstrat

35 eterodimeric proteins, using interleukin 23 (IL-23) as a model.

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

37 th SNPs in the IL-23R or the interleukin-23 (IL-23) cytokine itself and related downstream signaling

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

39 dence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA,

40 mab, a specific inhibitor of interleukin-23 (IL-23) via IL-23 p19 subunit binding, significantly impr

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

42 The interleukin-23 (IL-23)/T-helper 17 cell pathway is implicated in psoriat

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

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

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

46 osis, proliferation, and activation by IL-7, IL-23, and IL-12 by cell culture, flow cytometry, and ph

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

48 After IL-23 gene transfer, wild-type mice exhibited concurrent

49 reased the potential to produce IL-17A after IL-23 stimulation.

50 ogether, these results suggest that although IL-23 is dispensable for GC formation, it is essential t

51 Guselkumab, an IL-23 inhibitor that specifically binds the IL-23 p19 su

52 rmacodynamic model as well as efficacy in an IL-23 and IL-12-dependent mouse colitis model.

53 development of psoriasiform dermatitis in an IL-23 intradermal injection model.

54 ng in loss of ILC3s from the intestine in an IL-23-dependent manner and exacerbating colitis.

55 IL-23 expression and skin inflammation in an IL-23-dependent model of psoriasis.

56 nd demonstrated biologic-like efficacy in an IL-23-induced preclinical model of psoriasis.

57 Thus, in an IL-23-mediated model that allows concurrent assessment o

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

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

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

61 ssion of the p40 subunit shared by IL-12 and IL-23 (IL-12/23p40).

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

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

64 Since IL-12 and IL-23 are related cytokines that share the common p40 su

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

66 Interleukin (IL)-12 and IL-23 belong to the IL-12 type family and are composite

67 IL-12 and IL-23 blockade with anti-IL-12p40 treatment completely e

68 ytes produce elevated inflammatory IL-12 and IL-23 in a GSK3alpha/beta-dependent manner upon TLR stim

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

70 dicates that neutralization of the IL-12 and IL-23 pathways does not ameliorate disease.

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

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

73 l directly suppress TYK2-dependent IL-12 and IL-23 signaling and Janus kinase 1-dependent signaling i

74 Importantly, binding of IL-12 and IL-23 to IL-12Rbeta1 is mediated by p40, and binding to

75 Complementation of IL-12 and IL-23 was able to restore T cell differentiation both in

76 antibody to p40, blocks cytokines IL-12 and IL-23, and is a highly effective and safe treatment for

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

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

79 dii infection that is dependent on IL-12 and IL-23.

80 te IL-12 family members, including IL-12 and IL-23.

81 mma receptor IIB; dual blockade of IL-12 and IL-23; and inhibition of Janus kinases.

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

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

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

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

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

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

88 eria stimulated Myd88-dependent IL-1beta and IL-23 production from myeloid cells, inducing proliferat

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

90 cytokine expression, including IL-1beta and IL-23, was also higher than in healthy controls, but bot

91 duction of cytokines, including IL-1beta and IL-23.

92 -producing cells in response to IL-1beta and IL-23.

93 7A and IFN-gamma in response to IL-1beta and IL-23.

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

95 de antigens or stimulation with IL-1beta and IL-23.

96 transcriptionally amplify TNF, IL-1beta, and IL-23 production by human inflammatory macrophages.

97 ducing cytokines, such as TNF, IL-1beta, and IL-23, is particularly dependent on IgG2, whereas type I

98 emonstrates that interleukin (IL)-1beta- and IL-23-prime T cells that express pathogenic T(Eta)17 sig

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

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

101 recurrence (serum IL-17A, IL-17F, IL-22, and IL-23) after withdrawal were evaluated.

102 r, IL-6, IFN-gamma, IL-12, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophilic esophagi

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

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

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

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

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

108 ally, in humans, the Th17 cytokines IL-6 and IL-23 associate with severe CDI, and patients with high

109 17-instructing cytokines IL-1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell differentiation was

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

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

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

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

114 L-12Rbeta1.IL-12Rbeta2 receptor complex, and IL-23 uses also IL-12Rbeta1 but engages IL-23R as second

115 inflammation induced by imiquimod (IMQ) and IL-23 and tested the effect of inhibiting LAT1 (JPH203)

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

117 inical success of therapies blocking TNF and IL-23 in IBD and in some forms of SpA.

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

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

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

121 nt compared with ustekinumab treatment (anti-IL-23/-IL-12).

122 or DC-specific deficiency in XBP1 attenuated IL-23 expression and skin inflammation in an IL-23-depen

123 activity in activated T cells via autocrine IL-23 signaling.

124 t a molecular determinant of balance between IL-23 and IL-12 expression, potentially governing immune

125 The relationships between IL-23 blockade, serum markers downstream of IL-23 signal

126 mall-molecule inhibitor of TYK2 that blocked IL-23 signaling in vitro and inhibited disease progressi

127 lity in the induction of IL-17A and IL-22 by IL-23.

128 17 cells, and its expression was enhanced by IL-23-signal transducer and activator of transcription 3

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

130 tory skin disease that is mainly mediated by IL-23, IL-1beta, and IL-17 cytokines.

131 -1R1-deficient T cells was fully restored by IL-23 polarization and expansion in vitro Therefore, our

132 Adenoviral gene transfer of a single-chain IL-23 induces psoriatic arthritis-like symptoms in NOD m

133 n or inhibition of LAT1 efficiently controls IL-23- and IL-1beta-induced phosphatidylinositol 3-kinas

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

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

136 Another proinflammatory cytokine, IL-23, is critical for the development of Th17 cells, wh

137 We herein hydrodynamically delivered IL-23 minicircle DNA into wild-type and CCR6-deficient (

138 bunit, we also evaluate the effect of direct IL-23 blockade on the development of AAA.

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

140 Dysregulated IL-23/IL-17 responses have been linked to psoriatic arth

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

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

143 T cells from WD-fed mice exhibited enriched IL-23 receptor expression and increased the potential to

144 inducible in GD-OF, cells failing to express IL-23.

145 emonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processe

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

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

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

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

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

151 hich can still form functional heterodimeric IL-23.

152 CD103(-) DC predominate in PDA, express high IL-23 and TGF-beta, and induce FoxP3(neg) tumor-promotin

153 However, IL-23 roles have not been studied in this infection.

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

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

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

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

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

159 n important contribution of Mon/Mac cells in IL-23 related skin inflammation and suggest that these c

160 gammadelta T cells are key effector cells in IL-23-mediated skin and joint inflammation in mice.

161 The role of CCR6, however, in IL-23-mediated joint inflammation is unclear.

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

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

164 3 subunits causing a cytokine milieu rich in IL-23 to favour Th2 polarization.

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

166 onoclonal autoantibody, M22, robustly induce IL-23 in human fibrocytes; however, IL-12 expression is

167 fects were associated with failure to induce IL-23 and IL-6, two key IL-22 inducers in the early and

168 TYK2 pseudokinase domain, potently inhibits IL-23 and IFNalpha signaling in cellular assays.

169 Guselkumab selectively inhibits IL-23 and in psoriasis, produces high clinical responses

170 noclonal antibody that specifically inhibits IL-23 by binding the cytokine's p19 subunit, was efficac

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

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

173 n galectin-8-knockout mice after intradermal IL-23 treatment than in wild-type mice.

174 se model of psoriasis induced by intradermal IL-23 injections and in IL-17A-treated keratinocytes.

175 invariant NKT cell numbers as well as lower IL-23 levels.

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

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

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

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

180 Herein, we discuss the known biology of IL-23 at the human enthesis and highlight the remarkable

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

182 Blockade of IL-23 pathway with either anti-p40 or anti-p19 subunits

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

184 ow that a deficiency of the p19 component of IL-23 in the autoimmune BXD2 (BXD2-p19(-/-) ) mouse lead

185 Correlation of IL-23 signaling serum cytokines increased with disease r

186 IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice.

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

188 unity has translated into the development of IL-23- and IL-17A-blocking antibodies for the treatment

189 IL-23 blockade, serum markers downstream of IL-23 signaling, and withdrawal were explored with gusel

190 The dysregulation of IL-23 pathways and bile acid pathways may be key to the

191 neonate mice is accompanied by elevation of IL-23 and IL-22 and decreased production of pancreatic e

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

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

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

195 a support the use of selective inhibition of IL-23 to treat psoriatic arthritis.

196 , a murine model of intradermal injection of IL-23 was used.

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

198 how that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease t

199 is was not due to high circulating levels of IL-23, as transgenic animals and controls had similar le

200 SAP reduced serum levels of IL-23, IFN-beta, MCP-1, and tumor necrosis factor-alpha,

201 yzed skin resident Tregs in a mouse model of IL-23 mediated psoriasiform dermatitis.

202 ncluding efficacy studies in mouse models of IL-23-driven acanthosis, anti-CD40-induced colitis, and

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

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

205 -driven ILC3 loss, whereas overexpression of IL-23 induces loss of ILC3s in the absence of GM-CSF.

206 the eye and that systemic overexpression of IL-23 resulted in a severe experimental SpA, confirmed a

207 6-knockout) mice to induce overexpression of IL-23 systemically.

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

209 could be identified as the main producers of IL-23 in LPS-stimulated PBMCs.

210 se results show that augmented production of IL-23 and IL-22 in early life has a negative impact on p

211 study, we investigated why the production of IL-23, a key mediator of inflammation in autoimmunity, i

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

213 Here, we examined the role of IL-23 in diabetes in nonobese diabetic mice.

214 h disease recurrence, supporting the role of IL-23 in expansion and maintenance of CD4+ T helper type

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

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

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

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

219 immunity through intracellular signaling of IL-23.

220 mab, and brodalumab), and the p19 subunit of IL-23 (guselkumab, tildrakizumab, risankizumab, and miri

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

222 lammatory cytokines, with the suppression of IL-23 being the most prominent.

223 cell responses partially via suppression of IL-23 receptor expression.

224 particularly effective in the suppression of IL-23-driven autoimmunity.

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

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

227 of IL-7R, responded less to IL-7, IL-12, or IL-23 cytokines, and were more prone to apoptosis compar

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

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

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

231 e results show that blockade of IL-12 and/or IL-23 may transiently reduce AVI, with more durable redu

232 Blockade of GM-CSF or IL-23 reverses anti-DR3 antibody-driven ILC3 loss, where

233 are mirrored in neonate mice overexpressing IL-23 in CX3CR1(+) myeloid cells or in keratinocytes.

234 estores normal growth in mice overexpressing IL-23.

235 has four members, which are IL-12 (p40:p35), IL-23 (p40:p19), the p40 monomer (p40), and the p40 homo

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

237 icacy of anti-IL-12p40 treatment may reflect IL-23 blockade.

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

239 adenoviral vector encoding single-chain (sc)IL-23 (Ad.scIL-23) was able to induce systemic antitumor

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

241 ammat(+) iNKT and gammadelta-hi T cells show IL-23 mediated Th17-like immune responses and were clear

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

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

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

245 ion, and secretion of Th1 (IL-12)- and Th17 (IL-23, IL-1beta, and IL-6)-conditioning cytokines by mye

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

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

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

249 Our results demonstrate that IL-23 drove the accumulation of Tregs; including a subpo

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

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

252 Collectively, our data shows that IL-23 drives Treg plasticity by inducing a population of

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

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

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

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

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

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

259 IL-23 inhibitor that specifically binds the IL-23 p19 subunit, significantly and safely improved pso

260 53 ameliorated skin inflammation in both the IL-23-induced ear swelling model and the topical imiquim

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

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

263 transduction downstream of receptors for the IL-23/IL-12 pathways and type I interferon family, where

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

265 A dysregulation in the IL-23/IL-17 axis can lead to inflammation of barrier tis

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

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

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

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

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

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

272 Activation of the IL-23/IL-17 pathway is integral to the development of ps

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

274 ase that develops under the influence of the IL-23/T helper 17 cell axis and is characterized by inte

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

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

277 Intriguingly, although targeting the IL-23-IL-17 axis substantially improves psoriasis outcom

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

279 We find that the IL-23 alpha-subunit remains partially unstructured until

280 r (TCR) stimulation, T cells upregulated the IL-23 receptor and the IL-23alpha p19 subunit, but not t

281 yte/macrophage (Mon/Mac) population when the IL-23 pathway is activated, a murine model of intraderma

282 ranscriptomic biomarkers associated with the IL-23 pathway, which were maintained through 8 weeks.

283 arcinogenesis was accompanied by an IL-12 to IL-23 shift with a consecutive development of a T(h)2/GA

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

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

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

287 CCR6-knockout mice were resistant to IL-23-induced skin inflammation but exhibited no changes

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

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

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

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

292 ific inhibitor of interleukin-23 (IL-23) via IL-23 p19 subunit binding, significantly improved psoria

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

294 In vitro, IL-23 drove the generation of CD4(+)Foxp3(+)RORgammat(+)

295 both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease.

296 Treatment of Il1rl2 (-/-) mice with IL-23 during the early phase of C. rodentium infection r

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

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

299 to a distinct transcriptomic signature with IL-23 as hallmark.

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