ライフサイエンスコーパス: IL-22

1 IL-22 ameliorates liver fibrosis by inhibiting hepatic s

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

3 IL-22 and IL-17A derive from both independent and overla

4 IL-22 binding protein (IL-22BP, IL-22Ra2) is a soluble i

5 IL-22 contributes to both chronic inflammatory and infec

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

7 IL-22 has been shown to have hepatoprotective effects th

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

9 IL-22 is critical for the maintenance of intestinal barr

10 IL-22 is expressed by activated lymphocytes and is impor

11 IL-22 may also cause inflammation and abnormal cell prol

12 IL-22 not only augmented the expression of Il18 mRNA and

13 IL-22 receptor engagement is necessary and sufficient to

14 IL-22 stimulates the epithelial cells via the IL-22RA1-I

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

16 IL-22 treatment increased expression of miR-200a and dec

17 IL-22 treatment on Caco-2 monolayers and on primary huma

18 IL-22 was rapidly induced in the lung during pneumococca

19 IL-22- and IL-17-positive T cells were sorted from human

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

21 IL-22-IL-22R signaling plays a crucial role in regulatin

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

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

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

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

26 es in serum cytokines and chemokines (IL-13, IL-22, CCL17) were found in AD versus healthy individual

27 Cytokines (IL-12p40, IL-13, IL-22, CCL17, CCL18, peptidase inhibitor 3 [PI3]/elafin,

28 tory and barrier markers (keratin 16, IL-13, IL-22, CCL17, CCL18, PI3/elafin, S100As, and loricrin).

29 ed with increased expression of IL-4, IL-13, IL-22, thymic stromal lymphopoietin, and other cytokines

30 ar cytokines (i.e. IL-5, IL-13, IL-9, IL-17, IL-22).

31 a role for EGR2 in the regulation of IL-17, IL-22, IL-28A, and TNF-beta cytokines in GBS patients.

32 TC17 cells, and TH17 cells producing IL-17, IL-22, or both, which activate mononuclear phagocytes bu

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

34 r the induction of interleukin 17A (IL-17A), IL-22, and IL-23 in the tongue after infection, as well

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

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

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

38 The combined increase in IL-17A/IL-22 results in enhanced epithelial cell activation and

39 -23 stimulation, cosecreting IL-17A, IL-17F, IL-22, GM-CSF, and IFN-gamma.

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

41 Interleukin 22 (IL-22) is an IL-10-related cytokine produced by T helper

42 in deficiency of intrathymic interleukin-22 (IL-22) compared with transplant recipients without GVHD,

43 nnate lymphoid cells produce interleukin-22 (IL-22) in response to loss of double positive thymocytes

44 Interleukin-22 (IL-22) is released by immune cells and mediates strong h

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

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

47 and driving them to produce interleukin-22 (IL-22).

48 In the presence of IL-23, IL-22 production is independent of aryl hydrocarbon rece

49 ignificant portion of the steady-state IL-23/IL-22 axis.

50 ecretion of autocrine/paracrine IL-10, IL-4, IL-22 and thymic stromal lymphopoietin regulated these J

51 tissue and increased concentrations of IL-6, IL-22, TNF-alpha, and IL-10.

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

53 sis and psoriasis pathology through abundant IL-22 production, whereas group 1 innate lymphoid cells

54 Accordingly, IL-22 was shown to promote liver regeneration upon acute

55 is for therapeutic interventions that affect IL-22 production by targeting IL-1 activity.

56 in was decreased in fibrotic rat liver after IL-22 treatment.

57 ted and secreted TH1/TH2 cytokines alongside IL-22 after drug stimulation.

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

59 eir endogenous IL-23 production and drive an IL-22 response in naive CD4(+) T cells that mediates epi

60 ing and polarizes human skin DCs to drive an IL-22 response, supporting the utility of IL-23 and IL-2

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

62 ping, a surrogate for scratching, induces an IL-22 response that drives epidermal hyperplasia and ker

63 cells that produced the cytokines IL-17 and IL-22 (TH17 cells).

64 The role of interleukin (IL)-17 and IL-22 in GVHD remains uncertain, due to an apparent lack

65 Importantly, the frequency of IL-17(+) and IL-22(+) CD4(+) T cells increased in the spleen of LPS-e

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

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

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

69 , with decreased pro-inflammatory IL-17- and IL-22-producing T cells.

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

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

72 restingly, combined inhibition of IL-17A and IL-22 did not worsen abscesses but did increase gamma in

73 n the clinic, high levels of both IL-17A and IL-22 expression are present in the skin of patients wit

74 ed, in correlation with increased IL-17A and IL-22 expression in inflamed skins.

75 fied dual roles for the cytokines IL-17A and IL-22 in bovine tuberculosis, where they show potential

76 Concentrations of IL-17A and IL-22 increased in milk at the onset of the inflammatory

77 ial IL-17A-positive cells and BAL IL-17A and IL-22 levels were similar in children with STRA and cont

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

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

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

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

82 characterized by high amounts of IL-17A and IL-22.

83 hypothesis that interleukin-17A (IL-17A) and IL-22 play distinct roles in immunity to cutaneous and i

84 h increased production of IL-10, IL-17A, and IL-22 compared with patients colonized with non-USA300 s

85 s, as IL-1alpha, IL-1beta, IL-6, IL-17A, and IL-22 were significantly elevated in fungal-exposed Il1r

86 eceptor (ROR) gammat, IFN-gamma, IL-17A, and IL-22, all hallmarks of type 3 innate lymphoid cells, we

87 okine secretion assays detecting IL-17A- and IL-22-producing cells in a single purification step.

88 om memory T cells, and decreased IL-17A- and IL-22-producing human and murine gammadelta and NKT cell

89 the IL-23 aptamer decreased both IL-17f and IL-22 by approximately 45% but did not result in signifi

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

91 ing in significantly upregulated IL-17f, and IL-22; topical application of the IL-23 aptamer decrease

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

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

94 ing lineages, defined as T helper (Th)22 and IL-22(+) Th17 cells.

95 esponse, supporting the utility of IL-23 and IL-22 blockade in AD.

96 ally injured skin and caution that IL-23 and IL-22 blockade in patients with AD may enhance susceptib

97 panied by inhibition of IFN-gamma, IL-4, and IL-22 compared with wells containing pDMECs treated with

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

99 s include KGF, use of the cytokines IL-7 and IL-22, and hormonal modulation including growth hormone

100 cells and higher expression of TNF-alpha and IL-22 were observed in mice carrying a deletion of Nod2

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

102 se correlation between miR-323-3p levels and IL-22 production in PBMCs cultured in T-cell growth cond

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

104 ISA were performed to quantify Il22 mRNA and IL-22 protein in mouse and human skin.

105 in induced local expression of Il22 mRNA and IL-22 protein.

106 y and resistance to S. aureus pneumonia, and IL-22 protects against severe pulmonary staphylococcal i

107 of pro-inflammatory Th17 cell responses, and IL-22 production enhanced LRC colonization in the steady

108 Donor Th22 and IL-22(+) Th17 cells share a similar IL-6-dependent devel

109 nylated surface of the target cell, and anti-IL-22 and IL-17A detection antibody labelled with a fluo

110 ed cytokine secretion assay consists of anti-IL-22 and anti-IL-17A catch antibodies, which via biotin

111 Because IL-22 can be dual-natured, we hypothesized that its biol

112 suggesting there may be a crosstalk between IL-22/STAT3 and beta-catenin pathway.

113 y aimed to investigate the interplay between IL-22 and miR-200a in regulating liver fibrosis in vivo

114 ession ratio reflects the level of bioactive IL-22 in psoriasis skin, we found positive correlations

115 Importantly, while both IL-22 and IL-17 mediate skin GVHD, Th17-induced chronic

116 e cytokines, we have utilised a novel bovine IL-22 specific recombinant antibody for flow cytometry.

117 17-induced chronic GVHD can be attenuated by IL-22 inhibition in preclinical systems.

118 y number (CN) variation and its induction by IL-22-remains unclear.

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

120 mune cells that regulate tissue responses by IL-22 production.

121 th AD with skin infections had higher CD4(+) IL-22(+) and IL-17(+) cell frequencies, which were highl

122 We show that in CD4 T cells IL-22 expression is upregulated in hypoxia.

123 were highly significant among CLA(-) cells (IL-22: 3.7 vs 1.7 [P < .001] and IL-17: 1.7 vs 0.6 [P <

124 ss significant effects among CLA(+) T cells (IL-22: 11 vs 7.5, P = .04).

125 identifies a role for liver NK1.1(+) cells, IL-22 and CpG oligonucleotides in the induction of toler

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

127 Constitutive IL-22 expression was dependent on the microbiota and MyD

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

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

130 inhibitor of the tissue-protective cytokine IL-22.

131 ence of ILC3s or the ILC3 signature cytokine IL-22.

132 The cytokine IL-22 helps to orchestrate this three-way interaction.

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

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

135 Inflammatory cytokines IL-22, IL-17a, IL-1beta, gamma interferon (IFN-gamma), a

136 tors, P2X1 and P2Y6, significantly decreased IL-22 secretion ex vivo.

137 bition of P2X1 was associated with decreased IL-22 secretion, elevated liver injury, and impaired liv

138 study shows that innate immune cell-derived IL-22 is required for efficient liver regeneration and t

139 We demonstrate that donor T cell-derived IL-22 significantly exacerbates cutaneous chronic GVHD a

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

141 group 3 innate lymphoid cell (ILC3)-derived IL-22.

142 h22 differentiation assay and generated dual IL-22/IL-17A reporter mice to isolate and compare pure p

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

144 on S. pneumoniae Taken together, endogenous IL-22 and hepatic IL-22R signaling play critical roles i

145 y amplifying inflammation-induced epithelial IL-22 signaling to STAT3.

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

147 Exogenous IL-22 protected mice from S. aureus pneumonia.

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

149 ts of IL-22BP expression but still expressed IL-22.

150 ILC1s, interleukin (IL)-13(+) ILC2s, and for IL-22(+), but not for IL-17A(+) ILC3s.

151 mensal bacteria and innate in nature, as for IL-22-related pathways.

152 Furthermore, GATA-3 was required for IL-22 production in both ILC3 subsets.

153 ed AHR ligands were selectively required for IL-22 production.

154 since its discovery in 2000, and a role for IL-22 has been identified in numerous tissues, including

155 ed mice, demonstrating a pathogenic role for IL-22 in the colon.

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

157 We generated IL-22 reporter mice to assess production of this key cyt

158 Bovine tuberculin (PPDB) induced greater IL-22 and IL-17A production in Mycobacterium bovis (M. b

159 High IL-22 levels in cultures correlated with protection agai

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

161 lation and characterization of viable, human IL-22-producing CD4+ T cells that do not produce IL-17A.

162 -deficient CD4 T cells, we show that hypoxic IL-22 upregulation is dependent on HIF-1alpha.

163 Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic

164 Hence, the ILC-IL-22 axis is essential in protecting against gut barrie

165 Manipulation of the ILC-IL-22-TEC axis may be useful for augmenting immune recon

166 Age strongly impaired IL-22 responses, and genetic studies identified several

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

168 wed the highest expression for miR-323-3p in IL-22- and IL-17-double-positive T cells and its capacit

169 atment reversed the Abeta-induced changes in IL-22 and IL-17 and the ratio of Bax/Bcl-2.

170 -181a, miR-26a, and miR-874 were detected in IL-22-producing T cells.

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

172 was associated with a profound reduction in IL-22 expression, particularly by colonic neutrophils.

173 fering RNA reverses the reduction of TEER in IL-22-treated cells.

174 The pivotal function of Tyk2 in IL-22-dependent colitis was confirmed in Citrobacter rod

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

176 bilizer of HIF-1alpha at normoxia, increased IL-22 expression.

177 dies and extend the observation of increased IL-22 and IL-17A responses in M. bovis-infected animals

178 on when challenged as adults, with increased IL-22-producing gammadelta(+) T cells.

179 nized mechanism by which cancer cells induce IL-22 production from memory CD4(+) T cells via activati

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

181 is known to act on CD4(+) T cells to induce IL-22 production.

182 In these settings, IL-1 induced IL-22 production from a mixed T helper cell population c

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

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

185 ctively, in addition to its role in inducing IL-22 production, macrophage-derived or CD103(-) CD11b(+

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

187 ranscription factor HIF-1alpha may influence IL-22 expression.

188 recipients without GVHD, thereby inhibiting IL-22-mediated protection of thymic epithelial cells (TE

189 ctivity should be tightly regulated to limit IL-22 expression to the sites of inflammation.

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

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

192 ele of rs2227473 produced significantly more IL-22 than those without this allele.

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

194 Moreover, IL-22-mediated upregulation of Claudin-2 and loss of TEE

195 h IL-22BP can control deleterious actions of IL-22 in the skin, its limited production prevents a suf

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

197 In a mouse model of PH, deletion of IL-22 was associated with significantly delayed hepatoce

198 owever, little is known about the effects of IL-22 on the regulation of tight junctions in the intest

199 Thus, we hypothesized that enhancement of IL-22 signaling would control pneumococcal burden in lun

200 LR9 agonist (ODN 1585) enhances expansion of IL-22-producing CD3-NK1.1(+) cells in the liver and prol

201 homeostasis by regulating the expression of IL-22 and the antimicrobial peptides RegIIIbeta, RegIIIg

202 ly, IL-18 was required for the expression of IL-22 in innate lymphoid cells (ILCs) upon T. gondii inf

203 ism to stimulate CD4(+) T cell expression of IL-22 without upregulating IL-17.

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

205 positive correlations with the expression of IL-22-inducible molecules (IL-20, IL-24, IL-36gamma, CXC

206 This paper presents the findings of IL-22 signaling during a murine model of pneumococcal pn

207 d MPhi and LDC infiltration and induction of IL-22, CRAMP, and mbetaD-3.

208 The inhibition of IL-22 led to a reduction in IL-17A expression, but not v

209 IL-22BP, IL-22Ra2) is a soluble inhibitor of IL-22 that regulates IL-22 activity.

210 Knowledge of IL-22 biology has evolved rapidly since its discovery in

211 Here, we found that plasma levels of IL-22 and its upstream cytokine, IL-23, are highly eleva

212 of sfb, as demonstrated by higher levels of IL-22 and larger numbers of IL-22(+) TCRbeta(+) cells an

213 The levels of IL-22 are elevated in AD skin lesions.

214 Serum levels of IL-22, a cytokine known to induce keratinocyte prolifera

215 tion prevents a sufficient neutralization of IL-22 and contributes to the development and maintenance

216 Neutralization of IL-22 prevented the development of colonic, but not ceca

217 higher levels of IL-22 and larger numbers of IL-22(+) TCRbeta(+) cells and neutrophils in BALF.

218 We found that overexpression of IL-22 or therapeutic administration of recombinant IL-22

219 Additionally, the percentages of IL-22-producing ILCs were reduced in the absence of diet

220 (-) mice, we show that the main producers of IL-22 post-PH are conventional natural killer cells and

221 CD1a-reactive T cells inducing production of IL-22 and IL-17A.

222 lanted mice is involved in the production of IL-22 and in the reduced inflammatory response to allogr

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

224 th factor-beta pathway and the production of IL-22 in T cells.

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

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

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

228 local barrier defense via mucosal release of IL-22 and calprotectin.

229 of ILCs could be improved by restoration of IL-22 signaling.

230 The role of IL-22 and IL-22BP in chronic liver diseases is unknown.

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

232 We sought to determine the role of IL-22 in the clearance of S aureus infection of mouse sk

233 novel mechanistic insights into the role of IL-22 in the regulation and maintenance of the intestina

234 However, the role of IL-22-IL-22R is understudied in Streptococcus pneumoniae

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

236 ent liver regeneration and that secretion of IL-22 in the regenerating liver is modulated by the ATP

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

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

239 Group 3 ILCs (ILC3s) are innate sources of IL-22 and IL-17 and include lymphoid tissue-inducer (LTi

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

241 ctivation and inhibition of either IL-17A or IL-22 leads to disease amelioration.

242 of IFN-gamma, TNF-alpha, IL-2, IL-17, and/or IL-22 in CD4 T cells and IFN-gamma-expressing CD8 T, gam

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

244 racterized by overproduction of IL-18 and/or IL-22.

245 autoantibodies, neutralizing anti-IL-17 or -IL-22 Abs, or gastrointestinal symptoms, although scarci

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

247 by which human ILC3s proliferate and produce IL-22, and identify NF-kappaB as a potential therapeutic

248 imination between Th17 cells that co-produce IL-22 and single IL-22-producing Th22 cells has not been

249 T cells are the main immune cells to produce IL-22 in the liver, a process mediated by the IL-23/phos

250 and IL-23 stimulate T cell subsets producing IL-22, another direct target of AHR transactivation.

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

252 d the expansion of the pathogen by promoting IL-22 production from the group 3 innate lymphoid cell (

253 or therapeutic administration of recombinant IL-22 (rIL-22), given 2 h postinfection, significantly r

254 n (TSLP) by IECs, which negatively regulated IL-22 production by ILC3s and impaired innate immunity t

255 a soluble inhibitor of IL-22 that regulates IL-22 activity.

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

257 tor agonist, which was sufficient to restore IL-22 expression and promote full recovery from DSS-indu

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

259 ected in patients, who also had higher serum IL-22 levels that were positively correlated with hBD-2

260 Finally, we observed that serum IL-22/IL-22BP protein ratio strongly correlated with pso

261 Th17 cells that co-produce IL-22 and single IL-22-producing Th22 cells has not been possible until t

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

263 In M. bovis-infected animals, PPDB specific IL-22 and IL-17A responses were observed in both CD4+ T

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

265 ndent mTOR activity also induced spontaneous IL-22 and IFN-gamma production, but these cytokines had

266 Furthermore, the strong IL-22 increase in lesional psoriatic skin was accompanie

267 Consequently, 1,25D suppressed IL-22, IL-17F, and GM-CSF production from tonsillar and

268 lling pneumococcal lung burden, and systemic IL-22 decreases bacterial burden in the lungs and periph

269 red increased TH2/TC2/IL-13(+) and TH22/TC22/IL-22(+) populations (P < .1) in patients with severe AD

270 the TH2 (IL-13, IL-31, and CCL17) and TH22 (IL-22 and S100As) axes and some TH1 skewing (IFN-gamma a

271 exacerbates cutaneous chronic GVHD and that IL-22 is produced by highly inflammatory donor CD4(+) T

272 We concluded that IL-22 inhibits HSC activation and ameliorates liver fibr

273 These results demonstrate that IL-22, through IL-22Ra1 and STAT3 singling, can induce i

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

275 We hypothesized that IL-22 regulation would occur at the interface between ca

276 We observed that IL-22 significantly reduced the proliferation of HSC and

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

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

279 These findings show that IL-22 is important for limiting the growth of S aureus o

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

281 nary pneumococcal infection, suggesting that IL-22 signaling in the liver is important to control pne

282 ida infection is negatively regulated by the IL-22/NLRC4/IL-1Ra axis.

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

284 while Th22 cells arise independently of the IL-22(+) Th17 lineage, IL-17 signaling to donor Th22 dir

285 Hypothesizing that the IL-22/IL-22BP expression ratio reflects the level of bio

286 that Tyk2 deficiency can be rescued via the IL-22 receptor complex.

287 f transcription (JAK/STAT) signaling via the IL-22 receptor, resulting in enhanced tumor-promoting in

288 Among them, IL-22 largely contributes to epithelial remodeling and i

289 Therefore, IL-22 may be a useful adjunct in treating hepatic and in

290 fects of NK1.1(+) cells are mediated through IL-22 production, which enhances allograft survival and

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

292 cytokines were detected in both cell types, IL-22/IL-17A double producers were rare and confined mai

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

294 nia and improvement of bacterial burden upon IL-22 administration.

295 ells and other immune cells that signals via IL-22 receptor alpha 1 (IL-22Ra1), which is expressed on

296 However, it is unclear whether IL-22 can directly regulate antimicrobial programs in th

297 However, it remains unclear whether IL-22 is critical for the crosstalk between liver lympho

298 ithin 2 days of infection and coincided with IL-22-dependent upregulation of the epithelial tight jun

299 Furthermore, serum from mice treated with IL-22 had improved opsonic capacity by increasing C3 bin

300 o studies also showed that mice treated with IL-22 had increased C3 expression in the liver compared