ライフサイエンスコーパス: IL-9

1 IL-9 deficiency suppressed acute and chronic colitis.

2 IL-9 fate reporter mice established type 2 innate lympho

3 IL-9 is a pleiotropic cytokine involved in various (path

4 IL-9 is a proallergic cytokine produced by a newly propo

5 IL-9 is important for the growth and survival of mast ce

6 IL-9 is produced by T cells, natural killer T cells, mas

7 IL-9 production by ILCs depended on IL-2 from adaptive i

8 IL-9 receptor (IL-9R)-deficient mice displayed reduced n

9 IL-9 was first described in the late 1980s as a member o

10 IL-9(+) cell numbers decreased from 102 to 71 per hpf (P

11 IL-9, a hematopoietic growth factor, is considered to be

12 IL-9, IL-10, and IL-17RB expression in vivo was inhibite

13 IL-9-blocking antibodies reversed this tumor growth inhi

14 IL-9-producing Th9 cells have been associated with autoi

15 IL-9-secreting (T(H)9) T cells are thought to represent

16 IL-9-secreting T cells develop in response to the combin

17 IL-9-secreting Th9 cells are the most recent Th subset t

18 IL-9-secreting Th9 cells have been considered to play a

19 IL-9/Th9 can function as both positive and negative regu

20 uction of the Th2 cytokines IL-5 (p = 0.02), IL-9 (p < 0.01), and IL-13 (p < 0.01), but had no effect

21 uction of anti-inflammatory cytokines IL-10, IL-9, IL-13, and VEGF-alpha in a beta-catenin- and PPARg

22 x vivo in a cytokine (interleukin-12 [IL-12]/IL-9/IL-15)-dependent manner, while acute-type ATL perip

23 ometry was used to measure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T

24 y cell subsets, as well as IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines, defining TH1/cytotoxic

25 Th17/Th22 polar cytokines (i.e. IL-5, IL-13, IL-9, IL-17, IL-22).

26 vitro in the presence of TGF-beta and IL-15, IL-9 was the most abundant among 16 analyzed cytokines a

27 n ICOS agonist cosecreted heightened IL-17A, IL-9, and IFN-gamma, their therapeutic effectiveness was

28 The cytokines IFN-gamma, IL-4, IL-17A, IL-9, and PU.1, a Th9 associated transcription factor, w

29 nstitutively activates interleukin-2 (IL-2), IL-9, and IL-15 autocrine/paracrine systems that in turn

30 leukemic cells cultured alone produced IL-2/IL-9, and the downstream Janus kinase/signal transducer

31 ed with TCR engagement: IL-12, IL-18, IL-27, IL-9, IL-25, and TGF-beta1.

32 he presence of KITLG and the cytokines IL-3, IL-9, and IL-6 promoted the development of a single popu

33 f kit ligand (KITLG) and the cytokines IL-3, IL-9, and IL-6 under serum-free conditions, or by KITLG

34 reduced nasal fluid concentrations of IL-4, IL-9 and eotaxin (all P < 0.05, 8 h level and/or area un

35 and soluble factors, including IL-21, IL-4, IL-9, and IFN-gamma.

36 and decreased production of IFN-gamma, IL-4, IL-9, and IL-17A in cells subjected to T-helper differen

37 , interferon gamma-induced protein 10, IL-4, IL-9, IL-10, fibroblast growth factor 2, IL-7, IL-15, an

38 e type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 have important roles in stimulating innat

39 roduces the canonical type 2 cytokines IL-5, IL-9 and IL-13 in response to IL-25 and IL-33.

40 and Gata3, they mature to give rise to IL-5, IL-9 and IL-13 producing ILC2.

41 and secretion of the type 2 cytokines IL-5, IL-9 and IL-13 that was dependent on cell-intrinsic expr

42 e type-2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13, are essential for the control of parasit

43 heir expression of interleukin (IL)-4, IL-5, IL-9 and IL-13, are required for immunity to helminth pa

44 d activation of T cells and release of IL-5, IL-9, and GM-CSF in the BAL fluid of mice, indicating an

45 ion of the chemokine CCL11, as well as IL-5, IL-9, and IL-13 in NH cells, thus attracting eosinophils

46 diators, including prostaglandin D(2), IL-5, IL-9, and IL-13, are also in clinical trials and might b

47 kines, including interleukin-4 (IL-4), IL-5, IL-9, and IL-13, drive the characteristic features of im

48 and produce the type 2 cytokines IL-4, IL-5, IL-9, and/or IL-13.

49 sed levels of anti-inflammatory (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and TGF-beta) cytokine

50 of anti-inflammatory cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and transforming growt

51 ion of multiple cytokines (IL-2, IL-4, IL-5, IL-9, IL-10, IL-17, IL-21, IL-22, IFN-gamma, and TNF) an

52 kines, including interleukin-4 (IL-4), IL-5, IL-9, IL-13, IL-31, and thymic stromal lymphopoietin (TS

53 ction of gamma interferon (IFN-gamma), IL-5, IL-9, IL-17, and IL-22 and decreased production of IL-10

54 pression of IL-1alpha, IL-1beta, IL-2, IL-6, IL-9, IL-10, IL-12(p70), IL-13, TNF-alpha, IFN-gamma, gr

55 11, CCL4, CCL25 and down-regulation of IL-6, IL-9, IL-10, IL-27, IFNA4, CSF3, LOC100152038, and LOC10

56 tokines, including interleukin (IL)-2, IL-7, IL-9, and IL-15.

57 amma-chain, gamma(c), with IL-2, IL-4, IL-7, IL-9, and IL-15.

58 Along with IL-4, IL-7, IL-9, IL-15, and IL-21, IL-2 shares the common cytokine

59 rleukin (IL) receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21.

60 mma(c) leading to the loss of IL-2/IL-4/IL-7/IL-9/IL-15/IL-21 signaling and a lack of NK and mature T

61 red with CD4(+)LAP(-) T cells, secrete IL-8, IL-9, IL-10, IFN-gamma, and TGF-beta upon activation, an

62 transcription factor PU.1 and interleukin 9 (IL-9) in patients with ulcerative colitis.

63 Interleukin 9 (IL-9) is a cytokine linked to lung inflammation, but its

64 Interleukin 9 (IL-9) is a gammac-family cytokine that is highly produce

65 Interleukin 9 (IL-9) is a pleiotropic cytokine that can regulate autoim

66 Although the cytokine interleukin 9 (IL-9) was discovered decades ago, it remains one of the

67 red for the development of an interleukin 9 (IL-9)-secreting subset of helper T cells.

68 cytokines, 'alarmins' such as interleukin-9 (IL-9) and interleukin-33 (IL-33), and stress molecules i

69 positive association between interleukin-9 (IL-9) and TSLP concentration in the serum of infants wit

70 g Atg3 or Atg5 have increased interleukin-9 (IL-9) expression upon differentiation into TH9 cells rel

71 elevant biological sources of interleukin-9 (IL-9) have remained a mystery.

72 o investigate the role of Th9/interleukin-9 (IL-9) in the pathogenesis of hepatic fibrosis.

73 Interleukin-9 (IL-9) is a T cell cytokine that acts through a gammaC-fa

74 e and humans, a population of interleukin-9 (IL-9)-producing T cells activated via the ST2-IL-33 path

75 d by the potent production of interleukin-9 (IL-9).

76 estinal anaphylaxis driven by interleukin-9 (IL-9).

77 nd IL-23 receptor (IL-23R) produced abundant IL-9, and we found substantial growth inhibition of B16F

78 to map the fate of cells that have activated IL-9.

79 th Irf4 and Batf deficiency deeply affecting IL-9 production.

80 or curcumin diminished PU.1 expression after IL-9-inducing stimulation.

81 cues, namely TGF-beta and IL-4, adopting an IL-9-producing NKT cell phenotype able to mediate proinf

82 d2 ligation regulated clinical disease in an IL-9-dependent fashion.

83 of Atg5 have reduced tumour outgrowth in an IL-9-dependent manner.

84 scription were further demonstrated using an IL-9 luciferase reporter assay in which BCL6 repressed S

85 hmatics suppressed IFN-gamma (P = 0.015) and IL-9 (P = 0.023) less efficiently.

86 expressed interleukin-10 (IL-10), IL-13, and IL-9 and could migrate into adjacent compartments.

87 ated naive cells did not coexpress IL-17 and IL-9, unless they were repeatedly stimulated under Th17

88 make TNF and IFN-gamma, as well as IL-17 and IL-9.

89 s of IFN-gamma-, IL-22-, IL-13-, IL-17-, and IL-9-producing CD4(+) and CD8(+) T cells were compared i

90 Depletion of IL-17A and IL-9 had little impact on antitumor Tc17 cells activated

91 protein-1alpha (MIP-1alpha), MIP-1beta, and IL-9, as well as IL-10, more commonly considered an anti

92 r level of IL-17A, IL-17F, IL-21, IL-22, and IL-9, suggesting that endogenous IFN-beta suppresses the

93 e the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration o

94 lls, expressed high levels of the IL-9R, and IL-9 signaling was crucial for the survival of activated

95 crine manner to promote STAT5 activation and IL-9 production.

96 ical and nonredundant role for Th9 cells and IL-9 in host-protective type 2 immunity against parasiti

97 umour response that depends on Th9 cells and IL-9 induced by dectin-1-activated DCs in vivo.

98 Herein, we generated IL-9-deficient and IL-9-fluorescent reporter mice that demonstrated an esse

99 IL-1beta, gamma interferon (IFN-gamma), and IL-9.

100 reduction in innate lymphoid cell, ILC2, and IL-9(+) and IL-13(+) ILC2 numbers in the lung.

101 mice show reduced pulmonary inflammation and IL-9 production by T cells and innate lymphoid type 2 ce

102 cells is required for maximal pathology and IL-9 production in allergic lung inflammation.

103 stimulated IL-9 production in vivo, and anti-IL-9 treatment attenuated TSLP-induced airway inflammati

104 orrelated with the severity of AHR, and anti-IL-9 treatment decreased airway inflammation.

105 ch was exacerbated by NO and blocked by anti-IL-9 antibody.

106 Thus, anti-IL-9 mAb treatment may provide an effective therapeutic

107 e chemokine CCL17, which, in turn, attracted IL-9-producing T cells.

108 at Golgi transport inhibitors (GTIs) blocked IL-9 production.

109 Both IL-9 and IL-33 also promote lung mast cell infiltration

110 Both IL-9 and IRF4 expression are rescued by either IL-2 or c

111 (IL-4) control the differentiation of CD4(+) IL-9-producing helper T cells (TH9 cells) remain incompl

112 +), while only TSLP-mDCs promoted Th9 cells (IL-9 and PU.1+ /IRF4+).

113 f eosinophils, tryptase-positive mast cells, IL-9(+) cells, and mast cell-eosinophil couplets before

114 with EoE had significantly fewer mast cells, IL-9(+) cells, and mast cell-eosinophil couplets in the

115 man CD4(+) T cell subpopulation coexpressing IL-9 and IL-10, but not IL-4, the expansion of which is

116 Increased levels of IL-5, GM-CSF, IL-9, and IL-17A were also comparable in subjects with H

117 duction of the mast cell-activating cytokine IL-9.

118 cells that produce the pleiotropic cytokine IL-9.

119 The cytokine IL-9, derived primarily from T-helper 9 (Th9) lymphocyte

120 sociated with induced inflammatory cytokines IL-9, IL-17A and IFNgamma in response to Notch ligation

121 -55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN-gamma, causing an e

122 and chronic allergic inflammation, decreased IL-9 levels in mice with PU.1-deficient T cells correspo

123 deacetylase activity augments PU.1-dependent IL-9 production.

124 t sialostatin L suppresses mast cell-derived IL-9 preferentially by inhibiting IRF4.

125 ause we could show recently that Th9-derived IL-9 is essentially involved in the induction of asthma

126 contrast, IL-21 induced BCL6 and diminished IL-9 expression in wild-type but not Bcl6(-/-) cells, an

127 binding sites in the Il9 (the gene encoding IL-9) promoter.

128 Treatment of these cells with IL-25 enhances IL-9 expression in vitro.

129 mportantly, adoptive transfer of an enriched IL-9(+) iNKT cell population leads to exacerbated allerg

130 ic iNKT cells from naive mice do not express IL-9, iNKT cell activation in the presence of TGF-beta a

131 fraction of PICA-resistant T cells expressed IL-9 (T(H)9 cells).

132 ', that is the main cell type that expresses IL-9 in vivo.

133 To what extent IL-9-producing cells are induced or regulated by sensiti

134 cells that made the mast cell growth factor IL-9.

135 Bronchoalveolar lavage fluid IL-9 and IL-10, serum IL-9, and lung IL-17RB levels were

136 ance of these factors results in priming for IL-9 secretion, we examined the effects of each pathway

137 on and function and define a requirement for IL-9 in TSLP-induced allergic inflammation.

138 This highlights a unique role for IL-9 as an autocrine amplifier of ILC2 function, promoti

139 rred by recent work demonstrating a role for IL-9 in regulating inflammatory immunity and defining th

140 These results suggest a role for IL-9 in tumor immunity and offer insight into potential

141 l induced by CD200, with a critical role for IL-9, IL-35, and transforming growth factor-beta in the

142 ted reporter mouse to demonstrate a role for IL-9-secreting T cells in helminthic parasite immunity.

143 Hence, fostering IL-9-mediated ILC2 activation may offer a novel therapeu

144 mitogenic stimulation, but are distinct from IL-9(+) Th2 cells.

145 Functionally, IL-9 impaired intestinal barrier function and prevented

146 Herein, we generated IL-9-deficient and IL-9-fluorescent reporter mice that d

147 specific immune responses, here we generated IL-9-skewed CD8(+) T (Tc9) cells by priming with Th9-pol

148 require an immature mast cell that generates IL-9 to induce its own maturation.

149 e a cell therapy product that maintains high IL-9 expression in vivo while inhibiting IFN-gamma drive

150 However, IL-9 can also be secreted by mouse Th17 cells and may me

151 ll interfering RNA in human T cells impaired IL-9 production, whereas ectopic PU.1 expression promote

152 ad2 or Smad4 in T cells resulted in impaired IL-9 expression, which was coincident with enrichment of

153 le for the interferon regulatory factor-4 in IL-9 production.

154 with PU.1-deficient T cells have defects in IL-9 production from CD4(+) T cells, but not natural kil

155 IL-2 responses eliminates the difference in IL-9 production between wild-type and STAT3-deficient T

156 ranscriptional regulation of the Il9 gene in IL-9-expressing T cells and the relatedness of this subs

157 nt mast cells exhibit a strong impairment in IL-9 production, demonstrating the importance of IRF4 an

158 , the addition of TSLP led to an increase in IL-9 production from human and mouse Th9 cells, and indu

159 A resurgence of interest in IL-9 has been spurred by recent work demonstrating a rol

160 Increased IL-9 production in the absence of STAT3 correlates with

161 STAT3-deficient Th9 cells have increased IL-9 production that is maintained for longer in culture

162 ifferentiation, as deletion of Id3 increased IL-9 production from CD4(+) T cells.

163 ls known as Th9 cells that secrete increased IL-9 have been described.

164 lls of Th9 phenotype that secreted increased IL-9 and expressed a transcription factor profile charac

165 ed IL-6 supports a Th9 subtype by increasing IL-9 production, as observed in in vitro studies, or rat

166 ose that Notch and Smad3 cooperate to induce IL-9 and participate in regulating the immune response.

167 cooperated with TGF-beta signaling to induce IL-9.

168 In particular, DTA-1-induced IL-9 promoted tumor-specific cytotoxic T lymphocyte (CTL

169 IL-17RB in T cells results in IL-25-induced IL-9 production that is IL-4 independent.

170 ng soluble Notch ligand, Jagged2-Fc, induced IL-9 and IL-17A while delta-like 4Fc, another Notch liga

171 C2s) were major sources of infection-induced IL-9 production, the adoptive transfer of Th9 cells, but

172 in the presence of TGF-beta and IL-4 induces IL-9 secretion in murine and human iNKT cells.

173 hat during papain-induced lung inflammation, IL-9 production was largely restricted to innate lymphoi

174 L6-STAT5 binding competition that influences IL-9 production.

175 h9 cells, transcription factors that inhibit IL-9 production, and STAT6 is required for the induction

176 pha monoclonal antibody profoundly inhibited IL-9 expression, suggesting optimal expression of IL-9 w

177 n, with increased BCL6 expression inhibiting IL-9 production.

178 require IL-4 for induction of intracellular IL-9 expression.

179 ficient in both PU.1 and ETV5 there is lower IL-9 production than in cells lacking either factor alon

180 animal model, citrine reporter mice had more IL-9-expressing mucosal T cells in experimental oxazolon

181 ported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secre

182 ut they produce lower levels of IL-21 and no IL-9.

183 L-4, and STAT6 transcription factor, but not IL-9 signals.

184 h house dust mite, confirming the ability of IL-9-producing iNKT cells to mediate proinflammatory eff

185 In mice, the absence of IL-9 impaired ILC2 proliferation and activation of regul

186 tion was strongly impaired in the absence of IL-9 signaling.

187 Acquisition of IL-9 production was observed in different iNKT subsets d

188 MC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell prote

189 In addition, blockade of IL-9 or IL-4 enhanced allergen-specific IFN-gamma produc

190 Blockade of IL-9 production via neutralizing antibodies resulted in

191 review, we summarize the characterization of IL-9 biological activities, highlight roles for the cyto

192 L-17, resulted in the marked coexpression of IL-9 in IL-17 producing memory cells.

193 ges of Th9 and Th17 cells, concentrations of IL-9 and IL-17, as well as expression of IL-17, TNF-alph

194 ating monocytes were potent costimulators of IL-9 production by Th17 cells via their capacity to secr

195 ility of STAT5 to promote the development of IL-9-secreting T cells.

196 TR signaling enhanced the differentiation of IL-9-producing CD4(+) T-helper (TH9) cells in a TNFR-ass

197 roduction, which stimulates the emergence of IL-9(+) and IL-13(+) ILC2s and mast cells and leads to d

198 lasma concentrations and liver expression of IL-9 and IL-17A were significantly elevated in mice with

199 cells and was required for the expression of IL-9 and other Th9-associated genes in both human and mo

200 expression, suggesting optimal expression of IL-9 was dependent on IL-2 signaling in these patients.

201 ells in spleen, and suppressed expression of IL-9, IL-17A, IFN-gamma, TGF-beta1, IL-6, IL-4 and TNF-a

202 -/-)) mice, which have reduced expression of IL-9, were resistant to tumor growth inhibition by DTA-1

203 about the potential biological functions of IL-9 in the immune system and beyond.

204 nk between the well-established functions of IL-9 in the regulation of type 2 helper T cell cytokines

205 Given the pleiotropic functions of IL-9, Th9 cells might be involved in pathogen immunity a

206 However, following identification of IL-9-producing iNKT cells involved in mucosal inflammati

207 cient T cells, emphasizing the importance of IL-9 produced by T cells in mast cell recruitment.

208 nses is controversial, and the importance of IL-9- versus IL-4-producing CD4(+) effector T cells in t

209 ditions defined here for strong induction of IL-9 might be relevant for the development of Vdelta2 T-

210 regard to the unusual production kinetics of IL-9 and the short retention of these cells in affected

211 Lack of IL-9 enhanced tumor growth, while tumor-specific Th9 cel

212 IL-9 secretors demonstrate the same loss of IL-9 in subsequent rounds of differentiation.

213 The loss of IL-9 is not due to an outgrowth of cells that do not sec

214 The loss of IL-9 production correlates with increases in phospho-STA

215 netics suggest that regulatory mechanisms of IL-9 expression are shared by iNKT and CD4 T cells, with

216 Notably, neutralization of IL-9 considerably impaired tumor rejection induced by DT

217 Neutralization of IL-9 in mice ameliorated hepatic fibrosis, attenuated th

218 ritis in remission exhibited high numbers of IL-9(+) ILC2s in joints and the circulation.

219 -/-) and WT mice; however, the percentage of IL-9(+) CD4(+) T cells was increased in lung, bronchoalv

220 We identified a population of IL-9 and IL-10 coexpressing cells (lacking IL-4 expressi

221 Mutually exclusive production of IL-9 and the TH2-specific cytokine IL-5 suggests that th

222 statin L strongly inhibits the production of IL-9 by Th9 cells.

223 We demonstrate that production of IL-9 is increased in the absence of STAT3 and cytokines

224 Moreover, the per cell production of IL-9 is significantly higher in Th9 cells compared with

225 cells are specialized for the production of IL-9, promote allergic inflammation in mice, and are ass

226 , STAT3 functions as a negative regulator of IL-9 production through attenuation of STAT5 activation

227 Here we focus on the role of IL-9 and ILC2s during the lung stage of infection with N

228 We examined the role of IL-9/Th9 in a model of pulmonary melanoma in mice.

229 gulators of immune response, but the role of IL-9/Th9 in tumor immunity is unknown.

230 r secretion of IL-10 and higher secretion of IL-9 by casein-stimulated T cells were found in patients

231 The secretion of IL-9, initially recognized as a Th2 cytokine, was recent

232 However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to

233 TH9 cells are a major source of IL-9 in models of allergic inflammation and play an impo

234 Because eosinophils were one source of IL-9, they might support esophageal mastocytosis.

235 ficient mice, suggesting that the targets of IL-9 in this setting include mast cells but not T or B c

236 Breakthroughs made through the use of IL-9 reporter mice have allowed the identification of ce

237 The effects of STAT5 and BCL6 on IL-9 transcription were further demonstrated using an IL

238 ed therapeutic effect critically depended on IL-9 production in vivo.

239 Mast cell accumulation was dependent on IL-9, but not IL-13, a cytokine required for many aspect

240 therapeutic target in diseases dependent on IL-9.

241 Moreover, the effects of Gcn5 on IL-9 production are specific as the production of IL-10

242 cytokine receptors such as IL-7 receptor or IL-9 receptor, in which JAK1 is appended to the specific

243 ILC2s, emergence of a TSLP receptor-positive IL-9(+) ILC2 population, and an increase in intraepithel

244 his up-regulation was associated with potent IL-9 production as revealed by flow cytometry and multip

245 gene in cells that most efficiently produce IL-9.

246 itro, Itk(-/-) CD4(+) T cells do not produce IL-9 and have reduced levels of IRF4 (Interferon Regulat

247 he identification of cell types that produce IL-9 in vivo and, contrary to expectations based on prev

248 o permissive state, and therefore to produce IL-9 than did memory T cells.

249 ribed Th9 subset characteristically produces IL-9 and has been implicated in both allergy and autoimm

250 motes generation of murine T cells producing IL-9 (Th9) by signaling through DR3 in a cell-intrinsic

251 ently reported lines of Th9 cells, producing IL-9 and IL-10, were generated by polarization with IL-4

252 e predominant CD4(+) T cell subset producing IL-9 in the context of human infection.

253 on, whereas ectopic PU.1 expression promoted IL-9 production.

254 ansfer model demonstrated that TSLP promoted IL-9-dependent, Th9 cell-induced allergic inflammation b

255 ription factor ETS variant 5 (ETV5) promotes IL-9 production in Th9 cells by binding and recruiting h

256 cells that do not secrete IL-9, as purified IL-9 secretors demonstrate the same loss of IL-9 in subs

257 or growth, and administration of recombinant IL-9 (rIL-9) to tumor-bearing WT and Rag1(-/-) mice inhi

258 AT5 eliminates the ability of IL-6 to reduce IL-9 production.

259 of the expression of Gcn5 results in reduced IL-9 production.

260 Itk inhibition also reduces IL-9 expression by human T cells, implicating ITK as a k

261 rly defined, and outline questions regarding IL-9 functions that still require further exploration.

262 ion, the transcription factors that regulate IL-9 expression, and finally the potential roles for Th9

263 STAT5 and STAT6 regulated IL-9 expression by directly binding to the Il9 promoter.

264 TGF-beta-Smad2/4-signaling pathway regulates IL-9 production through an epigenetic mechanism.

265 transcription factor network that regulates IL-9 and demonstrated how combinations of cytokine signa

266 L-6, have the greatest potency in repressing IL-9 production in a STAT3-dependent manner.

267 cologic inhibition of EZH2 partially rescued IL-9 production in Smad-deficient Th9 cells.

268 ved immunosuppressor sialostatin L restrains IL-9 production by mast cells, whereas degranulation and

269 to an outgrowth of cells that do not secrete IL-9, as purified IL-9 secretors demonstrate the same lo

270 effector subsets are Th9 cells that secrete IL-9.

271 , memory CD4 T cells were induced to secrete IL-9 by simply providing TGF-beta during stimulation, as

272 oalveolar lavage fluid IL-9 and IL-10, serum IL-9, and lung IL-17RB levels were significantly increas

273 t not nonallergic controls, show significant IL-9 production in response to nickel.

274 e significantly reduced this nickel-specific IL-9 production.

275 sion was reflected in elevated Ag-stimulated IL-9 cytokine levels in whole blood culture supernatants

276 ic expression of TSLP in the lung stimulated IL-9 production in vivo, and anti-IL-9 treatment attenua

277 site Ag-driven Th2 (IL-4, IL-5, IL-13), Th9 (IL-9), and the regulatory (IL-10) cytokines when compare

278 LL37, and peptidase inhibitor 3/elafin), TH9/IL-9, IL-33, and innate markers (IL-8) than adults (P <

279 Our data suggest a deleterious role of Th9/IL-9 in increasing hepatic fibrosis and exacerbating dis

280 c stromal lymphopoietin, and periostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P <

281 hat is maintained for longer in culture than IL-9 in control cultures.

282 In this study, we demonstrate that IL-9 production is progressively lost in Th9 cultures du

283 This study demonstrates that IL-9, through its direct effects on Th1 and ability to p

284 We hypothesize that IL-9 also has a role in human allergic contact dermatiti

285 Here, we show that IL-9-expressing T cells generated in vitro in the presen

286 Intracellular cytokine staining showed that IL-9 and the TH2-specific cytokine IL-5 are produced by

287 The IL-9-secreting Th9 subset of CD4 Th cells develop in res

288 t a critical role for PU.1 in generating the IL-9-producing (T(H)9) phenotype and in the development

289 mental asthma, most likely by inhibiting the IL-9 production of Th9 cells.

290 A recent example of this paradigm is the IL-9-secreting Th9 cell that develops in response to TGF

291 TH2-specific cytokine IL-5 suggests that the IL-9-producing cells belong to the recently described TH

292 Thus, alternative to IL-9 neutralization sialostatin L provides the basis for

293 by treatment with neutralizing antibodies to IL-9.

294 colitis, whereas treatment with antibody to IL-9 suppressed colitis.

295 biological functions have been attributed to IL-9, it remains an understudied cytokine.

296 t functional subpopulations are receptive to IL-9 polarization.

297 vels of thymic stromal lymphopoietin (TSLP), IL-9, and IL-13, but not IL-5, in bronchoalveolar lavage

298 In contrast, BCL6 knockdown upregulated IL-9 production in Th9 cells.

299 A contact hypersensitivity model using IL-9(-/-) mice shows enhanced Th1 lymphocyte immune resp

300 Whether IL-9 serves an essential role in the initiation of host-

301 In contrast, treatment with IL-9 promoted ILC2-dependent Treg activation and effecti