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 has lent its numerical designation to the Th9 subse

4 IL-9 is a cytokine with pleiotropic functions, and it ha

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

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

7 IL-9 is an important mediator of allergic disease that i

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

9 IL-9 is produced by many cell types, including T cells,

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

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

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

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

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

15 IL-9-producing CD4(+) (Th9) cells are a subset of CD4(+)

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

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

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

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

20 re levels of the cytokines IFN-gamma, IL-13, IL-9, IL-17, and IL-22 in CD4(+)/CD8(+) T cells in the b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 ytokines implicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33.

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

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

39 ed allogeneic T cell proliferation and IL-5, IL-9, and IL-13 production compared with native Ab-treat

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

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

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

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

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

45 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

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

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

48 ding IL-1beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13, IL-17, CCL2, CCL3, CCL4,

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

50 11, CCL4, CCL25 and down-regulation of IL-6, IL-9, IL-10, IL-27, IFNA4, CSF3, LOC100152038, and LOC10

51 thways reduced the production of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, wit

52 -CSF), interleukin 1alpha (IL-1alpha), IL-6, IL-9, RANTES, tumor necrosis factor alpha (TNF-alpha), C

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

54 eptors for interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21.

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

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

57 arguing for a role for RA in interleukin 9 (IL-9) related diseases.

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

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

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

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

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

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

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

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

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

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

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

69 fibrotic T cell cytokines (IL-17, TNF-alpha, IL-9, and IFN-gamma) and chemokine receptors (CCR1, CCR2

70 s and chemokines, including IL-1, TNF-alpha, IL-9, CXCL1, CCL2, and CCL5 in the bronchoalveolar lavag

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

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

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

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

75 similar decreases in production of IL-13 and IL-9 by T cells, reduced mast cell accumulation and tiss

76 Th cells by IL-25 locally promoted IL-13 and IL-9 production.

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

78 lergic cytokines, including IL-5, IL-13, and IL-9 and decreased basophil activation.

79 CI, Salazar et al. show that while IL-17 and IL-9 induced distinct but complementary molecular pathwa

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

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

82 with NC had lower CSF tau, p-Tau(181) , and IL-9 levels in both living cohorts.

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

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

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

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

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

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

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

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

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

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

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

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

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

96 e interleukin (IL)-9 level and AD-associated IL-9 change to differ according to race, we performed im

97 Baseline and AD-associated IL-9 differences between African Americans and Caucasian

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

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

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

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

102 and IL-13, the resolution of inflammation by IL-9, IL-5-induced eosinophil expansion, IL-33-mediated

103 disease, and this worsening was inhibited by IL-9 neutralization.

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

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

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

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

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

109 y, AD was only correlated with increased CSF IL-9 levels in African Americans but not Caucasians.

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

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

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

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

114 hermore, key type 2 asthma-related cytokines IL-9 and IL-13, as well as additional immunomodulating c

115 s were reproduced by the signatory cytokines IL-9 and IL-17, with gene regulatory profiles evoked by

116 -55-specific Th9 cells resulted in decreased IL-9 production and induction of IFN-gamma, causing an e

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

118 Thus, our data demonstrate IL-9 production in mast cells and basophils in vivo requ

119 es Il9 CNS-25, and that Il9 CNS-25-dependent IL-9 production is required for mast cell expansion duri

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

121 We detected IL-9 levels and T(H)9 differentiation in patients with S

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

123 Calcitriol significantly diminished IL-9 secretion from murine Th9 cells associated with dow

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

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

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

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

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

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

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

131 ritical and cell type-specific component for IL-9 expression in BMMC.

132 Il9 CNS-25 is required for IL-9 production from T cells, basophils, and mast cells

133 BATF is required for IL-9 production in Th9 cells but in contrast to its func

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

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

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

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

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

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

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

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

142 low cytometry was used to measure IFN-gamma, IL-9, IL-13, IL-17, and IL-22 cytokine levels in CD4(+)/

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

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

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

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

147 In this study, we investigated how IL-9 modulates EAE development.

148 Yet, how IL-9 is regulated in mast cells or basophils is not well

149 However, IL-9 inhibited the IL-17A-mediated HPKs migration.

150 Finally, in addition to HPKs, IL-9 inhibited the migration of A-431 cells (epidermoid

151 This study group has previously identified IL-9-producing mucosal mast cell (MMC9) as the primary s

152 ve IgE production, followed by elevated IgE, IL-9, and IL-13 that maintain and enhance mast cell acti

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

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

155 ayed clearance in vivo, T cell deficiency in IL-9 also likely contributes to the phenotype.

156 s in a food allergy model, and deficiency in IL-9 expression results in decreased mast cell expansion

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

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

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

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

161 entiation because deleting Blimp-1 increased IL-9 production in CD4(+) T cells in vitro.

162 in response to TGF-beta plus IL-4 increased IL-9 expression and downregulated Blimp-1 expression com

163 Last, SMs also increased IL-9 and IL-13 production and, under competing condition

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

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

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

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

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

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

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

174 verexpression in human T(H)9 cells inhibited IL-9 expression.

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

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

177 es diminished early IL-21 induction and late IL-9 production, whereas exogenous IL-21 enhanced T(H)9

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

179 Mechanistically, IL-9 inhibited the IFN-gamma- and IL-17A-induced phospho

180 F convert Th17 cells into cells that mediate IL-9-dependent effects in allergic airway inflammation a

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

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

183 NF-kappaB but not TGF-beta-signaling negates IL-9 production by Th9(IL-4+IL-1beta) cells.

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

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

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

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

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

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

190 This was followed by the appearance of IL-9 and IL-13, cytokines known for their roles in mast

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

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

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

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

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

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

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

198 contradictory functions in the expression of IL-9 in murine Th9 cells and bone marrow-derived mast ce

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

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

201 ned activation of STAT5 on the expression of IL-9.

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

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

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

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

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

207 differing requirements for the induction of IL-9 production.

208 Accordingly, inhibition of IL-9 or IL-17 cytokines by neutralizing antibodies decre

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

210 histone deacetylase inhibitor), the level of IL-9 reached to the level of wild-type untreated Th9 cel

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

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

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

214 rker and downstream effector cell marker) of IL-9 upregulation only in African Americans but not Cauc

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 DR in Th9 cells attenuated the percentage of IL-9-secreting cells.

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

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

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

224 ever, selectively in BMMC, the production of IL-9 critically depends on autocrine IL-3 acting via the

225 is is our observation that the production of IL-9 in NFATc2-deficient Th9 cells is increased, whereas

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

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

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

229 istically with IL-1beta on the production of IL-9.

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

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

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

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

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

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

236 al mast cell (MMC9) as the primary source of IL-9 to drive intestinal mastocytosis and experimental I

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

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

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

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

241 therapeutic target in diseases dependent on IL-9.

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 Caucasians (n = 38), and analyzed postmortem IL-9-related gene expression profiles in the publicly av

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

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

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

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

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

250 s (producing IL-17) and Th9 cells (producing IL-9) exhibit functional plasticity, and their role in t

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

252 on of IL-1beta and IL-4 efficiently promoted IL-9-producing T cells (Th9(IL-4+IL-1beta)).

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

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

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

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

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

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

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

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

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

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

263 ference in STAT3 LOF cells partially rescued IL-9 differentiation.

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

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

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

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

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

269 Similarly, IL-9 inhibited the IFN-gamma-induced migration of HPKs b

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

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

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

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

274 Th17/IL-17 and Th9/IL-9 exhibit critical, but often opposing, roles in tumo

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

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

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

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

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

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

281 In this study, we describe that IL-9 profoundly reduced the actin stress fibers, inhibit

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

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

284 Our results suggest that IL-9 reduces autoimmune neuroinflammation by suppressing

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

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

287 er Th lineages and allows acquisition of the IL-9-secreting phenotype.

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

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

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

291 neuronal, and glial cells immunoreactive to IL-9, and quantitative analysis in independent US cohort

292 lysis for proteins mechanistically linked to IL-9 in brains of African Americans and Caucasians (n =

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

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

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

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

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

298 A key question before us now is whether IL-9 and IL-17 contribute to tumor progression in a sequ

299 However, the underlying mechanism by which IL-9 suppresses EAE has not been clearly defined.

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