ライフサイエンスコーパス: IL-22

1 IL-22 and IL-17, Bax and Bcl-2, PKA/PKG and the brain de

2 IL-22 contributes to both chronic inflammatory and infec

3 IL-22 frequencies serially increased from normal levels

4 IL-22 has been identified as a cancer-promoting cytokine

5 IL-22 has dual functions during tumorigenesis.

6 IL-22 is a dual natured cytokine which has context-depen

7 IL-22 is potentially a pathogenic cytokine in patients w

8 IL-22 signaling in HMA mice regulated host glycosylation

9 IL-22 single producing T cells, however, are not depende

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

11 IL-22, a downstream cytokine of IL-23, was highly increa

12 IL-22- and IL-17-producing T cells have important roles

13 IL-22-mediated host glycosylation thus fosters the growt

14 IL-22-mediated host N-glycosylation is likely impaired i

15 ro-inflammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF-alpha) and pronounced complement consumption,

16 0.99, 0.96, and 0.75 for IL-5, IL-6, IL-10, IL-22, and TNFalpha, respectively.

17 SCORAD correlated with immune (IL-13, IL-22) and epidermal (thickness, K16) measures in lesion

18 y volunteers also secreted IFN-gamma, IL-13, IL-22, and cytolytic molecules.

19 f cellular infiltrates and cytokines (IL-13, IL-22, and S100As) were similarly reduced only by steroi

20 rine/paracrine IL-10, TGF-beta, IL-4, IL-13, IL-22, and TSLP secretion and SOCS1/SOCS2/SOCS3 inductio

21 ory cells (Tregs) and interleukin 17 (IL-17)/IL-22-producing Th cells (Th17/Th22) from mucosal sites

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

23 , they upregulate T-bet and coexpress IL-17, IL-22, and IFN-gamma in a STAT3- and retinoic acid-depen

24 pha receptor, IL-6, IFN-gamma, IL-12, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophil

25 interleukin 1beta (IL-1beta), IL-13, IL-17, IL-22, and KC, and showed severe immune cell infiltratio

26 ticipants on the basis of longitudinal IL-17/IL-22 profiles identified discrete groups.

27 viduals distinguished by low levels of IL-17/IL-22 were linked to established markers of metabolic di

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

29 there is a decline in serum levels of IL-17/IL-22, with concomitant changes in the gut microbiome.

30 raction between the gut microbiome and IL-17/IL-22-producing cells plays a role in the development of

31 racterized by decreased diversity, and IL-17/IL-22-related declines in the phylum Firmicutes, class C

32 h the induction of interleukin-17A (IL-17A), IL-22, and gamma interferon (IFN-gamma) as well as the a

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

34 17/T helper type 22-related markers (IL-17A, IL-22, and S100A7/A8; P < 0.05) showed the highest reduc

35 n via PGE2 and regulation of the PGE2/IL-17A/IL-22 axis via IL-33 signaling during lung fungal exposu

36 stablishes novel mechanisms of innate IL-17A/IL-22 production via PGE2 and regulation of the PGE2/IL-

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

38 matory cytokines/chemokines (TNFa, IL-1beta, IL-22, IL-33, IL-17alpha, IL-2, MIP-2, and MCP-1), and n

39 tes DICER expression through canonical IL-20/IL-22 receptors.

40 ry cells and IL-17A(+), IL-17F(+), IL-21(+), IL-22(+), and IL-23(+) cells were examined by immunohist

41 es (interleukin-17A [IL-17A], IL-17F, IL-21, IL-22, and IL-26) in regulating the immune response to H

42 e T(H)2 (IL13, CCL17, and CCL26) and T(H)22 (IL-22) cytokines were significantly elevated in both AD

43 ficient in IFN-gamma but not interleukin 22 (IL-22) signaling pathways rescued chlamydial colonizatio

44 Interleukin 22 (IL-22) signals via both IL-22 receptor alpha1 (IL-22Ralp

45 -6), interleukin 10 (IL-10), interleukin 22 (IL-22), and tumor necrosis factor alpha (TNF-alpha).

46 red pneumonia worldwide, and interleukin-22 (IL-22) helps contain pneumococcal burden in lungs and ex

47 Interleukin-22 (IL-22) is a critical immune defence cytokine that mainta

48 The cytokine interleukin-22 (IL-22) is a critical regulator of epithelial homeostasis

49 Interleukin-22 (IL-22) plays an important role in host immunity and tiss

50 For example, interleukin-22 (IL-22) production by group 3 innate lymphoid cells (ILC3

51 with a nearly total loss of interleukin-22 (IL-22) production in the tonsil and colon; an increase i

52 n restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferation, and antimic

53 oliferation and ILC3-derived interleukin-22 (IL-22) production.

54 re we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymphoid cells (ILC3)

55 (+) ILC3 produced protective interleukin-22 (IL-22), whereas ILC1s produced proinflammatory interfero

56 ur studies revealed that the interleukin-22 (IL-22)/IL-17-producing ILCS was not altered during SIV i

57 stratify for high (n = 30) and low (n = 29) IL-22 expression groups.

58 IL-1 receptor antagonist anakinra abrogates IL-22 production and reduces tumor growth in a murine br

59 Although IL-22 deficiency did not affect skin disease development

60 Although IL-22 is produced by a variety of lymphocyte populations

61 Surprisingly, although IL-22 activates signal transducer and activator of trans

62 ous sensitization preferentially elicited an IL-22 response compared with intraperitoneal immunizatio

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

64 idative phosphorylation (OXPHOS) genes in an IL-22-dependent manner.

65 und to be due to downregulation of IL-12 and IL-22 cytokines.

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

67 elicited inflammation dependent on IL-17 and IL-22, thereby reducing CRC progression.

68 pro-inflammatory cytokines such as IL-17 and IL-22.

69 3 cytokines such as interleukin (IL)-17 and IL-22.

70 produce the type three cytokines, IL-17 and IL-22.

71 er rodentium is known to induce IL-17(+) and IL-22(+) CD4(+) T cells (T(h)17 and T(h)22 cells, respec

72 Production of interleukin-17 (IL-17) and IL-22 by T helper 17 (Th17) cells and group 3 innate lym

73 terferon (IFN-gamma), IL-5, IL-9, IL-17, and IL-22 and decreased production of IL-10 following IL-27

74 o measure IFN-gamma, IL-9, IL-13, IL-17, and IL-22 cytokine levels in CD4(+)/CD8(+) T cells, with ind

75 o measure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T cells.

76 cytokines IFN-gamma, IL-13, IL-9, IL-17, and IL-22 in CD4(+)/CD8(+) T cells in the blood of 19 patien

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

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

79 ng factors, including interferon, IL-17, and IL-22.

80 soriasis, and high frequencies of IL-17- and IL-22-expressing T cells in blood, correlating with seve

81 nhibitor decreased, the levels of IL-17A and IL-22 but not IL-1alpha, IL-1beta, or IL-6.

82 led a duality in the induction of IL-17A and IL-22 by IL-23.

83 IL-33-mediated regulation of IL-17A and IL-22 did not involve the modulation of IL-23 but rather

84 that IL-33-mediated regulation of IL-17A and IL-22 occurred at the level of PGE2 This was confirmed b

85 Impaired IL-17A and IL-22 production correlated with reduced invariant NKT c

86 RA-expressing cells and levels of IL-17A and IL-22 were quantified in BAL and biopsies and related to

87 , which attenuated fungal-induced IL-17A and IL-22, as well as IL-1alpha, IL-1beta, and IL-6, product

88 al mice attenuated fungal-induced IL-17A and IL-22, but not IL-1alpha, IL-1beta, or IL-6, production.

89 he autoimmunity-related cytokines IL-17A and IL-22.

90 12/15-LOX-dependent induction of IL-17A and IL-22.

91 Moreover, the TNF-alpha, IL-17A, and IL-22-induced phosphorylation of MAPK and JAK-STAT pathw

92 ly, chrysin reduced TNF-alpha-, IL-17A-, and IL-22-induced CCL20 and antimicrobial peptide release fr

93 amma, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22 using ELISA multiplex kit.

94 lpha, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22 were observed in CRC patients who received probiot

95 amma, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22) in patients with colorectal cancer.

96 rticular, TH17 cytokines IL-17A, IL-17F, and IL-22 was seen in PRP.

97 increased production of IL-17A, IL-17F, and IL-22, with the most striking enhancement in cells copro

98 ated with suppression of IL-17A, IL-17F, and IL-22.

99 T-cell subsets producing IL-17A, IL-17F, and IL-22.

100 Histamine, IL-6, IL-17, IL-21 and IL-22 induced the expression of H4R in monocytes.

101 ere treated with histamine, IL-17, IL-21 and IL-22, and a H4R antagonist (JNJ7777120), the gene expre

102 ice is accompanied by elevation of IL-23 and IL-22 and decreased production of pancreatic enzymes.

103 show that augmented production of IL-23 and IL-22 in early life has a negative impact on pancreatic

104 activated to produce interleukin (IL)-23 and IL-22, which promote antimicrobial peptide (AMP) product

105 ecretion through GATA binding protein 3, and IL-22 in turn improved the PCOS phenotype.

106 atinocyte growth factor, cytokines (IL-7 and IL-22), and hormonal modulation including sex steroid in

107 duced IFN-gamma also expressed TNF-alpha and IL-22.

108 was independent of TCRgammadelta T cells and IL-22.

109 fection with proliferation and IFN-gamma and IL-22 production.

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

111 ood (eg, inducible costimulator molecule and IL-22).

112 serum biomarkers (TARC, PARC, periostin, and IL-22), eotaxin-1, and eotaxin-3 significantly decreased

113 with moderate-to-severe AD treated with anti-IL-22 (fezakinumab) versus placebo (2:1) using transcrip

114 d by a secreted natural antagonist, known as IL-22 binding protein (IL-22BP), encoded by Il22ra2 To d

115 cell subset that produced IL-17A as well as IL-22, TNF, and IFNgamma, indicating a broad and substan

116 Because IL-22 blockade showed clinical efficacy only in patients

117 xpression of the IL-1 receptor, which boosts IL-22 secretion in response to IL-1beta.

118 Interleukin 22 (IL-22) signals via both IL-22 receptor alpha1 (IL-22Ralpha1) and the common IL-1

119 to the exaggerated immunopathology caused by IL-22 suppression, Salmonella burdens in the gut were re

120 ponse pathways were most strongly induced by IL-22.

121 between innate immune protection mediated by IL-22 and the efficiency of nutrient absorption.

122 ich antimicrobial responses are regulated by IL-22 and how IL-22 regulates the expression and product

123 The activity of IL-22 is regulated by IL-22 binding protein (IL-22BP); however, the expression

124 nal Th22-cell expansion that was reversed by IL-22 deletion or IL-6R inhibition.

125 of stress kinases, which can be reversed by IL-22 treatment via the induction of metallothionein.

126 production, and accumulation of CD3(+)CD4(+)IL-22(+) T cells that coexpressed IL-17A and TNF-alpha.

127 uced intestinal group 3 innate lymphoid cell IL-22 secretion through GATA binding protein 3, and IL-2

128 SCFAs promote human CD4(+) T cell IL-22 production.

129 r, although it does not target immune cells, IL-22 treatment attenuated the inflammatory functions of

130 ted cytokines, keratinocyte chemoattractant, IL-22, and IL-6, in plasma.

131 vestigate the role of IL-22BP in controlling IL-22 during skin inflammation, we used imiquimod-induce

132 role in acute liver damage, via controlling IL-22-induced Cxcl10 expression.

133 o date, the degree to which IL-22BP controls IL-22 in pulmonary infection is not well defined.

134 production of the cancer-promoting cytokine IL-22.

135 The cytokine IL-22 is rapidly induced at barrier surfaces where it re

136 The cytokine IL-22 plays a critical role in mucosal barrier defense,

137 2BP), an antagonist molecule of the cytokine IL-22.

138 Moreover, cytokines IL-22 or IL-17A induced increased activity of Yes-1.

139 related cytokines (e.g., TNF-alpha, IL17A-D, IL-22) in people with DS, independent of diagnosis of au

140 ata demonstrate a key role for donor-derived IL-22 in patients with chronic skin GVHD and confirm par

141 or ERK signaling and increased ILC3-derived IL-22 via an AKT and STAT3 axis.

142 ncy did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23

143 report that viral infection triggered early IL-22 production from the liver and lymphoid organs.

144 17066096 and the candidate gene that encodes IL-22 binding protein (IL-22BP), an antagonist molecule

145 ta indicate that IL-22BP deficiency enhances IL-22 signaling in the lung, thus contributing to resist

146 SCFA supplementation enhances IL-22 production, which protects intestines from inflamm

147 mic and splenic hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs.

148 espite uninhibited alloreactivity, exogenous IL-22 administration posttransplant resulted in increase

149 thermore, we showed that macrophages express IL-22 receptor subunit alpha-1 (IL-22Ra1) during pneumoc

150 elicited in the lungs Il22 mRNA expression, IL-22 production, and accumulation of CD3(+)CD4(+)IL-22(

151 tumorigenesis while excluding a function for IL-22 in transformed epithelial cells.

152 eline expression, suggest a central role for IL-22 in AD, indicating the need for a precision medicin

153 Our data reveal an unexpected role for IL-22 in promoting early tumorigenesis while excluding a

154 in T cells was necessary and sufficient for IL-22 production.

155 Moreover, data from IL-22 reporter mice show that most IL-22(+) cells in the

156 proinflammatory cytokines IL-17A, IFN-gamma, IL-22, and granulocyte-macrophage colony-stimulating fac

157 Here, IL-22 SyCyRs phenocopied native IL-22 signal transductio

158 lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer

159 rted by robust effects in patients with high IL-22 baseline expression, suggest a central role for IL

160 How IL-22 contributes to APC-mediated tumorigenesis is poorl

161 ial responses are regulated by IL-22 and how IL-22 regulates the expression and production of LCN-2 i

162 Our study demonstrates how IL-22-induced activation of STAT3 synergizes with NF-kap

163 recent advances in our understanding of how IL-22 regulates homeostasis and host defense, and we dis

164 s, exposure to cytokines TNFalpha, IFNgamma, IL-22, or IL-17A, resulted in compromised barrier functi

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

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

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

168 Ffar2 increased IL-22(+) CCR6(+) ILC3s and influenced ILC3 abundance in

169 t to S. pneumoniae infection, have increased IL-22 in lung tissues, and sustain longer survival upon

170 ering bile acid metabolism and/or increasing IL-22 levels may be of value for the treatment of PCOS.

171 lites, we assessed their potential to induce IL-22 expression by intestinal CD4(+) T cells.

172 Inulin-induced IL-22 expression, which required innate lymphoid cells,

173 cer cells of murine and human origin induced IL-22 production from memory CD4(+) T cells.

174 ngs establish the roles of SCFAs in inducing IL-22 production in CD4(+) T cells and ILCs to maintain

175 In acute and persistent viral infections, IL-22 deficiency resulted in thymic and splenic hypertro

176 Here, we show that Il22ra2 inhibits IL-22 during S. pneumoniae lung infection and that Il22r

177 To investigate IL-22 signalling in wild-type (WT) and APC-mutant cells,

178 th failure to induce IL-23 and IL-6, two key IL-22 inducers in the early and late phases of infection

179 human ILC3s, as well as induce and maintain IL-22 production.

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

181 Mechanistically, IL-22 acts directly at the level of pancreatic acinar ce

182 Mechanistically, IL-22 blocked hepatic oxidative stress and its associate

183 ents with severe AD, we used baseline median IL-22 mRNA expression to stratify for high (n = 30) and

184 Furthermore, IL-36R-mediated IL-22 production by CD4(+) T cells was dependent upon NF

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

186 data from IL-22 reporter mice show that most IL-22(+) cells in the colon 3 months after C. rodentium

187 Here, IL-22 SyCyRs phenocopied native IL-22 signal transduction, indicated by induction of cyt

188 tion of gamma interferon (IFN-gamma) but not IL-22 or antibody-mediated depletion of IFN-gamma from a

189 TNF-alpha, but not IL-22, blockade at the time of antigen inhalation challe

190 T recipients of T(H)22-polarized WT, but not IL-22-deficient, T-cell receptor OVA-specific T cells, w

191 Notably, IL-22-mediated keratinocyte-intrinsic MHC class II expre

192 nvironment improves, and genetic ablation of IL-22 restores normal growth in mice overexpressing IL-2

193 The activity of IL-22 is regulated by IL-22 binding protein (IL-22BP); h

194 Administration of IL-22 increases hepatic complement 3 and complement depo

195 Stem cells deprived of IL-22 signals and exposed to carcinogens escaped DDR-con

196 he first report showing a profound effect of IL-22 blockade on multiple inflammatory pathways in AD.

197 ermatitis (AD), but the molecular effects of IL-22 antagonism have not been defined in human subjects

198 aluate the cellular and molecular effects of IL-22 blockade in tissues from patients with moderate-to

199 The effects of IL-22 can be tempered by a secreted natural antagonist,

200 ically Th17 cells) promotes the emergence of IL-22-producing Th17 cells and thereby tumorigenesis in

201 ited significant impairment in expression of IL-22 and AMPs, increased intestinal damage, and failed

202 that associated with enhanced expression of IL-22-inducible antimicrobial peptides.

203 ctions of CD4 + T cells, higher fractions of IL-22, and a tendency to higher fractions of IL-17 produ

204 al adjacent tissue, whereas the frequency of IL-22 single producing cells is not changed.

205 Induction of IL-22 production correlated with the NIK-dependent reduc

206 Intranasal instillation of IL-22 with TNF-alpha, but not IL-17A, elicited neutrophi

207 est a pathogenic mechanism involving lack of IL-22-mediated inhibition of T cell-derived IFN-gamma ex

208 cosinolates produced only very low levels of IL-22 and, consequently, the DDR in epithelial cells of

209 ing is consistent with the reduced levels of IL-22 in individuals with PCOS.

210 ization results in increased serum levels of IL-22.

211 and AHR in WT mice, suggesting that loss of IL-22 synergy with TNF-alpha contributed to defective re

212 ng pathway was confirmed in a mouse model of IL-22-induced psoriasis-like dermatitis.

213 disease normally resolved, neutralization of IL-22 caused luminal narrowing of the cecum-a feature re

214 tion of IL-22, Ab-mediated neutralization of IL-22 did not abolish the protection from colitis in Nkx

215 teritis model, Ab-mediated neutralization of IL-22 impaired intestinal epithelial barrier integrity a

216 ation, suggesting a therapeutic potential of IL-22 in the context of MS.

217 ice and to test the therapeutic potential of IL-22 in this new NASH model.

218 hoid cells (ILC3s) as important producers of IL-22.

219 (mTORC1) for proliferation and production of IL-22 and IL-17A after in vitro activation and Citrobact

220 ng, in turn, ensures on-demand production of IL-22 by innate lymphocytes directly regulating componen

221 t of TGF-beta signaling on the production of IL-22 in CD4+ T cells is controversial.

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

223 delta T cells controlled their production of IL-22.

224 her studies suggest pathogenic properties of IL-22 during chronic liver injury.

225 Reconstitution of IL-22 at late time points through retransplantation into

226 However, the function and regulation of IL-22 in viral infection remain largely unknown.

227 tumor growth; therefore, tight regulation of IL-22 is essential.

228 hydrocarbon receptor, a master regulator of IL-22 production.

229 lls, we performed RNA sequencing (RNAseq) of IL-22-treated murine small intestinal epithelial organoi

230 We sought to determine the role of IL-22 in antigen-driven airway allergic inflammation aft

231 production and also identify a novel role of IL-22 in controlling antiviral T cell responses in the n

232 review, we focus specifically on the role of IL-22 in the intestinal epithelium.

233 The roles of IL-22 in the pathomechanisms of psoriasis have been well

234 delta2 T cells promoted mucosal secretion of IL-22 and ICOSL/TNF-alpha-dependent release of the IL-22

235 Th22 cells are a major source of IL-22 and have been found at sites of infection and in a

236 lation and were the major cellular source of IL-22 binding protein (IL-22BP) at steady state.

237 These cells expand and are a major source of IL-22 during secondary C. rodentium infection, even befo

238 ILC3s are a robust source of IL-22, a cytokine critical for stimulating the antimicro

239 lls, which are known to be a major source of IL-22, but the effect of TGF-beta signaling on the produ

240 and Th17 cells and enhanced transcription of IL-22, Ab-mediated neutralization of IL-22 did not aboli

241 Furthermore, treatment of IL-22 in mice upregulates Claudin-2 protein in colonic e

242 CN-2, has previously been shown to depend on IL-22, a cytokine produced by innate lymphoid cells type

243 f B cells, but not Foxp3(+) cells depends on IL-22.

244 blet cells do not depend on type I IFN or on IL-22 signaling, pathways responsible for protection aga

245 of IFN-gamma, IL-5 and IL-13, and IL-17A or IL-22, respectively.

246 ial cells were stimulated with IL-17A and/or IL-22, with and without budesonide.

247 ells exhibit low cytotoxic activity, produce IL-22, and have an expression profile that overlaps with

248 hoid cells (ILCs) and CD4(+) T cells produce IL-22, which is critical for intestinal immunity.

249 ived short-chain fatty acids (SCFAs) promote IL-22 production by CD4(+) T cells and ILCs through G-pr

250 ier defense, but the mechanisms that promote IL-22 expression in the human intestine remain poorly un

251 a AhR induction, and PI3K signaling promotes IL-22 production in Th17 cells.

252 testines; however, the factors that regulate IL-22 production by CD4(+) T cells and ILCs are not clea

253 of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also identify a novel role of IL-22

254 arly phase of C. rodentium infection rescued IL-22 production from group 3 innate lymphoid cells (ILC

255 administration during the late phase rescued IL-22-mediated production from CD4(+) T cell, and both t

256 weeks, respectively) than in the respective IL-22-high placebo-treated group (39.6% and 56.3% at 4 a

257 syndrome by nourishing microbiota to restore IL-22-mediated enterocyte function.

258 te signaling, homodimerization of the second IL-22 signaling chain, SyCyR(IL-10R2), which previously

259 Serum IL-22 levels are increased in patients with atopic derma

260 KT17 cell function while selectively sparing IL-22(+) subsets.

261 tion promotes generation of antigen-specific IL-22-producing T cells that promote airway inflammation

262 n of the naive T cells into antigen-specific IL-22-secreting cells.

263 ulating and skin-resident, antigen-specific, IL-22-secreting T cells are detectable in patients with

264 Specifically, IL-22 production was TYK2/JAK2/STAT3 dependent, while IL

265 17 cell-driven inflammation, they stimulated IL-22 secretion.

266 we demonstrate that MNV provides a striking IL-22-dependent protection against early-life lethal inf

267 Short term IL-22 production protects against genotoxic stress, wher

268 n epithelial stem cells, we demonstrate that IL-22 is required for effective initiation of the DDR fo

269 In summary, we have demonstrated that IL-22 signaling can be phenocopied by synthetic cytokine

270 In the present study, we found that IL-22 production in humans is dependent on activation of

271 acidifaciens Our findings thus indicate that IL-22 plays a protective role by limiting infection-indu

272 In this study we report that IL-22 signals exclusively through the basolateral side o

273 In summary, our results reveal that IL-22 increases intestinal epithelial permeability by up

274 We further show that IL-22 increases DNA damage and genomic instability, whic

275 Here, we show that IL-22 significantly decreased GJIC and down-regulated Cx

276 These results suggest that IL-22 decreases GJIC by activating the JNK signaling pat

277 Overall, these findings suggest that IL-22 is involved in the pathogenesis of CM.

278 AHR after antigen challenge, suggesting that IL-22 plays an important role in the atopic march.

279 The IL-22-induced down-regulation of Cx43 expression and dec

280 ostasis and host defense, and we discuss the IL-22 pathway as a therapeutic target in diseases of the

281 Furthermore, the IL-22-induced down-regulation of Cx43 expression mediate

282 provements were seen with fezakinumab in the IL-22-high drug-treated group (82.8% and 139.4% at 4 and

283 and ICOSL/TNF-alpha-dependent release of the IL-22 inducible antimicrobial protein calprotectin witho

284 el that enables sporadic inactivation of the IL-22 receptor in colon epithelial stem cells, we demons

285 nt to IL-22 due to reduced expression of the IL-22 receptor, and increased expression of inhibitors o

286 p (39.6% and 56.3% at 4 and 12 weeks) or the IL-22-low groups.

287 Cx43 overexpression effectively rescued the IL-22-induced decrease in GJIC in HaCaT cells.

288 T(H)22/IL22/S100A's, were restricted to the IL-22-high drug group (P < .05).

289 tion and disrupts STAT3 interaction with the IL-22 receptor.

290 ute to the defense against pathogens through IL-22 and IL-17 secretion.

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

292 ion of IL-22RA2 (which specifically binds to IL-22 and inhibits its activity), but not by the NF-kapp

293 The microbiota is central to IL-22 production in the intestines; however, the factors

294 ealed that ApcMin/Min cells are resistant to IL-22 due to reduced expression of the IL-22 receptor, a

295 at this effect is indeed due to uncontrolled IL-22 activity.

296 ainst genotoxic stress, whereas uncontrolled IL-22 activity promotes tumor growth; therefore, tight r

297 SCFAs upregulate IL-22 production by promoting aryl hydrocarbon receptor

298 stressors and promote epithelial repair via IL-22 and type I IFN signaling.

299 ection with S. pneumoniae, changes that were IL-22 dependent.

300 coexpression of inflammatory cytokines with IL-22 is linked to the ability of ILCs to coexpress T-be