ライフサイエンスコーパス: IL-33

1 IL-33 and ILC2 may also serve as biomarkers for disease

2 IL-33 drives augmented responses to ozone in obese mice.

3 IL-33 dysregulated lung Treg cells and impaired immunolo

4 IL-33 exhibited dynamic expression as levels normalized

5 IL-33 expression was detected in epithelial cells in col

6 IL-33 expression was detected in ex vivo-cultured primar

7 IL-33 is a member of the IL-1 family capable of inducing

8 IL-33 is an IL-1 cytokine superfamily member.

9 IL-33 is an instructive cytokine of type 2 inflammation

10 IL-33 plays an important role in the development of expe

11 IL-33 pretreatment increased not only the number of degr

12 IL-33 promoted marked changes in the expression of antim

13 IL-33 promotes innate and adaptive type 2 immunity and m

14 IL-33 protein was markedly overexpressed within the nucl

15 IL-33 receptor deficiency in Il4raF709 Il1rl1(-/-) mice

16 IL-33 receptor signaling and ILC2s were vital for the in

17 IL-33 signaling was dispensable during effector/challeng

18 IL-33, released during tissue injury in sepsis, activate

19 IL-33, required for viral clearance by cytotoxic T cells

20 IL-33-mediated regulation of IL-17A and IL-22 did not in

21 IL-33-positive basal epithelial cells expressed E-cadher

22 e involvement of alarmins such as IL-1alpha, IL-33, IL-16, and high-mobility group box 1 in cellular

23 Unlike IL-1beta, IL-33 does not have a signaling complex that includes bo

24 Mice were injected with anti-IL-25, IL-33 receptor, and/or TSLP mAbs before initial oral gav

25 Injection of an mAb to IL-25, IL-33 receptor, or TSLP strongly inhibited FA developmen

26 The pro-TH2 cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) are assoc

27 LTE4 enhanced the effect of PGD2, IL-25, IL-33, and TSLP, resulting in increased production of ty

28 interplay among the innate cytokines IL-25, IL-33, and TSLP.

29 to stimulation with a combination of IL-25, IL-33, thymic stromal lymphopoietin, and IL-2.

30 uction of IgE by B lymphocytes through IL-25/IL-33 stimulation or TLR triggering.

31 tate plus ionomycin, IL-25 plus IL-33 (IL-25/IL-33), or a mixture of Toll-like receptor ligands to ev

32 2-myristate 13-acetate plus ionomycin, IL-25/IL-33, or a mixture of TLR ligands.

33 Interleukin-33 (IL-33) has been subject of extensive study in the contex

34 through interference in the interleukin-33 (IL-33) pathway.

35 lated TLR4-dependent bladder interleukin-33 (IL-33) production.

36 une circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion via the activity of is

37 tions trigger the release of interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells)

38 Levels of IL-5, IL-33, and IL-28A/IFN-lambda2 were increased in multisen

39 f MRE11, but not depletion of ATM, abrogated IL-33 stimulation.

40 In vivo, recombinant HpARI abrogated IL-33, group 2 innate lymphoid cell (ILC2) and eosinophi

41 linking), or upon an innate-type activation (IL-33 stimulation).

42 l CCP module pair (CCP1/2), tethering active IL-33 within necrotic cells, preventing its release, and

43 PGE2 after fungal exposure when administered IL-33, suggesting that IL-33-mediated regulation of IL-1

44 by B cells is induced by the mucosal alarmin IL-33 (ref.

45 context of diseases triggered by the alarmin IL-33.

46 This shared signaling complex allowed IL-33 to induce the EGFR-mediated activation of the MAP-

47 expansion and eosinophilia but did not alter IL-33 induction.

48 Although IL-33 induces AP-1 and NF-kappaB, NFAT signaling has not

49 pression and that exogenous PGE2 can amplify IL-33 production via EP2 and EP4 receptors.

50 ygyrus Alarmin Release Inhibitor (HpARI), an IL-33-suppressive 26-kDa protein, containing three predi

51 d inflammatory response in the airways in an IL-33-dependent but TRL4-independent manner.

52 y (SCI), meningeal ILC2s are activated in an IL-33-dependent manner, producing type 2 cytokines.

53 ngly, both enzymes readily cleaved IL-18 and IL-33, two IL-1-related alarmins, as well as the cytokin

54 Although the IL-1beta and IL-33 complexes shared structural features and engaged i

55 uding those involving cytokines IL-1beta and IL-33.

56 T cells, thus we hypothesized that IL-2 and IL-33 cooperate to enhance Treg function.

57 e (IL233) bearing the activities of IL-2 and IL-33 for efficient targeting to Tregs.

58 ice express ST2, and coinjection of IL-2 and IL-33 increased the number of Tregs in lymphoid organs a

59 , which utilizes the cooperation of IL-2 and IL-33 to enhance Treg- and ILC2-mediated protection from

60 more efficiently than a mixture of IL-2 and IL-33.

61 DFE induced the expression of IL-25 and IL-33 by upregulation of IL-1 receptor-associated kinase

62 t show DFE-induced upregulation of IL-25 and IL-33.

63 immune response via the release of IL-25 and IL-33.

64 ion by blood ILC2s stimulated with IL-25 and IL-33.

65 LC2 gene expression in response to IL-25 and IL-33.

66 ulation with the alarmin cytokines IL-25 and IL-33.

67 n TSLP, but not the other alarmins IL-25 and IL-33.

68 of thymic stromal lymphopoietin, IL-25, and IL-33 at the epithelial barrier.

69 protein expression of TLR1, TLR6, IL-25, and IL-33 in human atopic dermatitis skin lesions with high

70 ted the expression of TLR1, TLR6, IL-25, and IL-33 in human primary keratinocytes and HaCaT cells.

71 Furthermore, we demonstrate that IL-4 and IL-33 promote up-regulation of PPARgamma in lung-residen

72 s only induced in the presence of GM-CSF and IL-33 via the p38-MK2/3 signaling module.

73 gnaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast cell activation are necessary for indu

74 th the highest interferon beta (IFNbeta) and IL-33 levels in the nasal pharyngeal fluids (NPF).

75 or the first time demonstrate that ILC2s and IL-33 signaling are regulated by miR-155 in allergic air

76 increased after challenge with both LTC4 and IL-33.

77 SP (0.01-1 muM) and IL-33 (1-100 ng/mL) in combination also greatly stimulat

78 by 30% (P < 0.05), when stimulated by SP and IL-33.

79 by 50% (P < 0.001) when stimulated by SP and IL-33.

80 IKB-alpha at 1 muM when stimulated by SP and IL-33.

81 ition, RV induced expression of both ST2 and IL-33 in airway epithelial cells.

82 Anti-IL-33 decreased rhinovirus replication and increased IFN

83 Anti-IL-33 decreased type 2 inflammation in all phases of dis

84 Anti-IL-33 or dexamethasone suppressed the magnitude of type

85 e diminished exacerbation severity, and anti-IL-33, but not dexamethasone, promoted antiviral interfe

86 ell IL-25 expression were attenuated by anti-IL-33 treatment and in TSLP receptor-knockout mice.

87 Interventions included anti-IL-33 or dexamethasone at various stages of disease.

88 duced acute exacerbation; however, only anti-IL-33 boosted antiviral immunity and decreased viral rep

89 us-infected human AECs, suggesting that anti-IL-33 therapy has the additional benefit of enhancing ho

90 We sought to determine whether anti-IL-33 therapy is effective during disease progression, e

91 s and healthy subjects and treated with anti-IL-33 after rhinovirus infection.

92 Treatment with anti-IL-33 or dexamethasone diminished exacerbation severity,

93 e of an innate immunologic stimulus, such as IL-33.

94 nstead to locally produced cytokines such as IL-33.

95 SSION: Ozone caused greater increases in BAL IL-33, neutrophils, and airway responsiveness in obese t

96 enge of Ptges(-/-) mice with aspirin blocked IL-33-dependent mast cell activation, mediator release,

97 Blocking IL-33 activity with a soluble ST2 receptor significantly

98 F-kappaB activations were necessary for both IL-33 production and PGE2 generation, and exogenous PGE2

99 effectively expanded in the mouse kidney by IL-33 treatment and are central regulators of renal repa

100 ecretion (P < 0.001) when stimulated only by IL-33, and ST2 receptor reduction also decreases SP-stim

101 study was to investigate the roles played by IL-33 in altering regulatory T (Treg) cells in the lungs

102 single-cell level and their potentiation by IL-33.

103 tory activity of ILC2s might be regulated by IL-33-elicited ST2(+) Tregs that also arise in immune-me

104 In bone marrow-derived dendritic cells, IL-33 induces the production of IL-6, IL-13, and TNF-alp

105 undantly expressed in lung epithelial cells, IL-33 plays critical roles in both innate and adaptive i

106 sis-surviving patients have more Treg cells, IL-33 and IL-10 in their peripheral blood.

107 anulocyte-colony stimulating factor (G-CSF), IL-33, IL-11, IL-1alpha, and IL-1beta.

108 The decrease in cutaneous IL-33 reduces REG3A expression in epidermal keratinocyte

109 S induced production of the type 2 cytokines IL-33 and IL-5, which promoted accumulation of eosinophi

110 Epithelial cytokines (IL-33, IL-25, and thymic stromal lymphopoietin [TSLP]) a

111 contributions of the other innate cytokines, IL-33 and thymic stromal lymphopoietin (TSLP), to the ob

112 hat, despite expansion of hepatic ILC2s, 3-d IL-33 treatment before Con A challenge potently suppress

113 antibiotic therapy associated with decreased IL-33 levels in the NPF and lower ST2 values in the bloo

114 er understand the role of epithelial-derived IL-33 in the intestinal tumorigenesis, we generated tran

115 The inability to detect IL-33 or TSLP, or to neutralize their activity, suggeste

116 4 (LTC4), given in combination with low-dose IL-33 to naive wild-type mice, led to synergistic increa

117 Elevated IL-33 levels and ILC2 responses were observed in the lun

118 In conclusion, elevated IL-33 signaling increases tumor development in the Apc (

119 In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which man

120 We discovered that endothelial IL-33 expression was stimulated as a response to adenovi

121 Exogenous IL-33 treatment revealed that miR-155 is needed for IL-3

122 nvestigated the role of epithelial expressed IL-33 during development of intestinal tumors.

123 sis, we generated transgenic mice expressing IL-33 in intestinal epithelial cells (V33 mice).

124 Finally, IL-33 enhanced ILC2 trafficking to the lungs in a parabi

125 LAD2 cells with a neutralizing antibody for IL-33 receptor, ST2, inhibits TNF secretion by 50% (P <

126 pensable for IL-4 induction, is critical for IL-33-driven Th2 effector function in type-2 allergic ai

127 Consistently, Apc (Min/+) mice deficient for IL-33 receptor (ST2), had reduced polyp burden.

128 reatment revealed that miR-155 is needed for IL-33-induced ILC2 expansion and eosinophilic airway inf

129 Here, we show that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the ex

130 Mice deficient in the receptor for IL-33 (Il1rl1(-/-)) unexpectedly demonstrated enhanced l

131 upregulated expression of the receptors for IL-33 and IL-25.

132 his study, we identified a critical role for IL-33, a hallmark peripheral ILC2-activating cytokine, i

133 These data reveal critical roles for IL-33 in the "atopic march" and will offer a new therape

134 Indeed, ILC2s from IL-33-challenged miR-155(-/-) lungs exhibited impaired p

135 Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibite

136 ated enhanced lung clearance of A. fumigatus IL-33 functioned as a negative regulator of multiple inf

137 r IL-33 in lung defense against A. fumigatus IL-33 was detected in the naive lung, which further incr

138 -like receptors (TLRs), macrophages generate IL-33, an IL-1 family member that induces innate immune

139 was associated with highly elevated hepatic IL-33 expression, severe liver inflammation, and infiltr

140 models in mice were used to investigate how IL-33 affects established immunologic tolerance in vivo.

141 HpARI bound directly to both mouse and human IL-33 (in the cytokine's activated state) and also to nu

142 In adaptive immunity, IL-33 interacts with dendritic cells, Th2 cells, follicu

143 In innate immunity, IL-33 and group 2 innate lymphoid cells (ILC2s) provide

144 e 2 responses are equivalently attenuated in IL-33- and LT-deficient mice, and optimal ILC2 activatio

145 phils and protection against EAE was lost in IL-33(-/-) mice and upon neutralization of IL-5.

146 However, the signaling pathways resulting in IL-33-induced effector functions of dendritic cells are

147 RV infection of 6-d-old mice increased IL-33 and TSLP protein abundance.

148 Ozone increases IL-33 in the lungs, and obesity augments the pulmonary e

149 AC are prerequisites for maximal LPS-induced IL-33 expression and that exogenous PGE2 can amplify IL-

150 to amplify NF-kappaB-dependent, LPS-induced IL-33 expression via exchange protein activated by cAMP

151 EP4 receptor agonist potentiated LPS-induced IL-33 generation from both mPGES-1-null and WT bmMFs, wh

152 EP2 receptors displayed reduced LPS-induced IL-33 levels.

153 ced systemic cytokines in vivo and inhibited IL-33-mediated cytokine release from human mast cells.

154 TGF-beta1 inhibited IL-33-mediated Akt and ERK phosphorylation as well as NF

155 Administration of intranasal IL-33 and TSLP was sufficient for mucous metaplasia.

156 Intratracheal IL-33 challenge resulted in decreased C5aR2 expression i

157 hese data demonstrate that an axis involving IL-33 and ILC2s is important for the development of asth

158 define a vital regulatory cascade involving IL-33, decidual B cells and PIBF1 in safeguarding term p

159 Mice lacking IL-33 signaling had normal development of ILC2s but reta

160 show that hematopoietic AR expression limits IL-33-driven lung inflammation through a cell-intrinsic

161 Mice lacking mPGES-1 showed lower IL-33 levels and attenuated lung inflammation in respons

162 miR-155(-/-) mice demonstrated impaired lung IL-33 levels in response to allergen challenge and the n

163 Human mature IL-33 is a member of the IL-1 family and a potent regula

164 2/3 signaling module is essential to mediate IL-33-induced cytokine production in dendritic cells.

165 tudy, we investigated the IL-1 family member IL-33 in lung defense against A. fumigatus IL-33 was det

166 Moreover, IL-33 increases NK-1 gene and surface protein expression

167 ammation in chronic stable asthma, and novel IL-33 inhibitors will need to block all biologically act

168 Airway administration of IL-33 with an antigen impaired immunologic tolerance in

169 Binding of IL-33 to the IL-33R induces activation of the canonical

170 ewed the current knowledge of the biology of IL-33 and discussed the roles of the IL-33 in regulating

171 diminished expression of the alpha-chain of IL-33 receptor on choriodecidual B cells and a lower lev

172 Moreover, disruption of IL-33 or IL-23 signaling attenuated cytokine-producing I

173 We illustrate the effect of IL-33 on mast cell biology at the single-cell level by s

174 eta1 also suppressed the combined effects of IL-33 and IgE-mediated activation on mouse and human mas

175 ice abrogated the tumor promoting-effects of IL-33 in the colon.

176 asthma, could further amplify the effects of IL-33 on ILC2 activation and lung inflammation.

177 ch may contribute to the observed effects of IL-33.

178 atment in mice led to sustained expansion of IL-33 receptor-positive kidney ILC2s and ameliorated adr

179 ce had significantly increased expression of IL-33 and IL-23, cytokines that promote ILC2 and ILC3, r

180 irway inflammation via induced expression of IL-33 by lung epithelial cells.

181 Mechanistically, downregulated expression of IL-33, a stimulator of type II innate lymphoid cells, in

182 in, we assessed the esophageal expression of IL-33, an epithelium-derived alarmin cytokine, in patien

183 entified a hitherto unrecognized function of IL-33 as a potent suppressor of innate antiviral immunit

184 Intravenous injection of IL-33 or pulmonary fungal allergen challenge mobilized I

185 We report that repeated injections of IL-33 during induction (early) and during development (l

186 rn infants were also collected and levels of IL-33 and type 2 cytokines were measured.

187 sions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile co

188 though plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endome

189 Higher expression levels of IL-33 in cadherin-11-deficient mice mediated ILC2 activa

190 his study therefore highlights modulation of IL-33, IgA, IL-1alpha, and the microbiota as a potential

191 Mechanistically, overexpression of IL-33 promoted expansion of ST2(+) regulatory T cells, i

192 antigen through the skin, in the presence of IL-33, developed antigen-specific airway inflammation wh

193 suppress effector T cells in the presence of IL-33.

194 Ralpha+ stromal cells are major producers of IL-33 in adipose tissue.

195 on reflected CysLT2R-dependent production of IL-33 by alveolar type 2 cells, which engaged in a bilat

196 ce displayed increased stromal production of IL-33, with concomitant enhancements in ILC2s and M2 mac

197 al infection via ILC-extrinsic regulation of IL-33 and IL-23.

198 ith receptor agonists induced the release of IL-33 and subsequent eosinophil infiltration into the lu

199 LC2s are poised to respond to the release of IL-33 upon liver tissue damage through expression of typ

200 e through several steps including release of IL-33, which promotes cytokine (IL-5, IL-13) production

201 suppression of TLR1 inhibited the release of IL-33.

202 We assessed the role of IL-33 in the augmented effects of ozone observed in obes

203 The role of IL-33 in the pathogenesis of allergic diseases is incomp

204 We investigated the role of IL-33 in the pathology of endometriosis using patient sa

205 nous PGE2 partly reversed the suppression of IL-33 production caused by p38 MAPK and NF-kappaB inhibi

206 ndicating that these cells can be targets of IL-33, and gammadelta T cell deficiency reduced obesity-

207 optosis, Fer-1 prevented the upregulation of IL-33, an alarmin linked to necroptosis, and other chemo

208 suggest new therapeutic approaches based on IL-33 and PIBF1 to prevent human PTL.

209 , we investigated the effects of TGF-beta on IL-33-mediated mast cell activation.

210 by IL-36, but not IL-1alpha/beta, IL-18, or IL-33.

211 hibited DFE-induced upregulation of IL-25 or IL-33.

212 Overall, IL-33 augmented IL-13 secretion from basophils cotreated

213 The effects of cysLTs, PGD2, IL-33, IL-25, TSLP, and IL-2 alone or in combination on

214 After the chronic phase, IL-33 levels were persistently high, and rhinovirus chal

215 istate 13-acetate plus ionomycin, IL-25 plus IL-33 (IL-25/IL-33), or a mixture of Toll-like receptor

216 ith neutralizing Abs to IL-33 or recombinant IL-33, IL-25, or TSLP.

217 ced inflammation or treated with recombinant IL-33.

218 Reduced IL-33 in the Sm Egg-inflamed environment was shown to co

219 h asthmatic and control children and reduced IL-33 levels in the airways of asthmatic children.

220 in TGF-beta1, beta2, or beta3 showed reduced IL-33-mediated production of TNF, IL-6, IL-13, and MCP-1

221 differences in ILC2 development and restores IL-33-mediated lung inflammation.

222 Serum IL-33 levels correlated significantly with serum levels

223 e to environmental allergens and less severe IL-33-driven lung inflammation, correlating with an impa

224 Thus, CysLT2R signaling, IL-33-dependent ILC2 expansion, and IL-33-driven mast ce

225 tor alpha chain, or treatment with a soluble IL-33 decoy receptor significantly reduced release of in

226 L-9)-producing T cells activated via the ST2-IL-33 pathway (T9IL-33 cells) increases GVL while decrea

227 ueous SRW extract (SRWe) directly stimulated IL-33 mRNA and protein expression by corneal epithelium

228 show that adenoviral transduction stimulates IL-33 expression in endothelial cells in a manner that i

229 T cell-mediated tissue damage and subsequent IL-33 release were responsible for the activation of hep

230 Subsequently, IL-33 administration to normal mice attenuated fungal-in

231 important, as TGF-beta1 injection suppressed IL-33-induced systemic cytokines in vivo and inhibited I

232 postnatal SHS exposure reversibly suppresses IL-33 levels in airspaces which, in turn, results in red

233 from which to design new therapies to target IL-33 signaling.

234 suggest therapeutic potential for targeting IL-33, ILC2s, and oxidative stress to prevent and/or tre

235 Our study suggests that targeting IL-33 may be an effective treatment for sepsis-induced i

236 Short-term IL-33 treatment in mice led to sustained expansion of IL

237 We conclude that IL-33 isoforms activate basophils and mast cells to driv

238 nate antiviral immunity and demonstrate that IL-33 contributes significantly to the synergistic inter

239 Collectively, these data demonstrate that IL-33 plays a critical role in promoting ILC2 egress fro

240 We demonstrate that IL-33 production by bone marrow-derived murine macrophag

241 ctively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion

242 dance with these observations, we found that IL-33 induced the emergence of a CD39(high) Treg populat

243 We found that IL-33 not only activated hepatic ILC2s but also expanded

244 Our data indicate that IL-33 contributes to augmented responses to ozone in obe

245 Together, these results indicate that IL-33-responsive ILC2s are an important link between the

246 We reasoned that IL-33 and TSLP expression are also induced by RV infecti

247 Here, we report that IL-33 (30 ng/mL), a member of the IL-1 family of cytokin

248 In this study, we report that IL-33 efficiently sustained the in vitro activation of V

249 Collectively, we report that IL-33 expression is induced in an undifferentiated, non-

250 idney-residing ILC populations revealed that IL-33 receptor-positive ILC2s are a major ILC subtype in

251 Here we show that IL-33 has a major function in the induction of this immu

252 ogy at the single-cell level by showing that IL-33 potentiates IgE-mediated mast cell responses by bo

253 s with allergic airway diseases suggest that IL-33 plays an important role in the pathogenesis of the

254 ure when administered IL-33, suggesting that IL-33-mediated regulation of IL-17A and IL-22 occurred a

255 The IL-33-activated transcriptome was enriched in genes comm

256 Additionally, the IL-33-positive cells had low expression of PCNA.

257 were pretreated with antibodies blocking the IL-33 receptor, ST2, and then exposed to ozone (2 ppm fo

258 The clinical findings that both the IL-33 and ILC2 levels are elevated in patients with alle

259 xp3(+) Treg cells in the lungs expressed the IL-33 receptor ST2.

260 (+) regulatory T cells (Treg) expressing the IL-33 receptor ST2 in the liver.

261 xpress cell surface molecules, including the IL-33 receptor, ST2, that are roughly comparable to thos

262 as observed in litters from dams lacking the IL-33 receptor, ST2.

263 Moreover, the IL-33-positive epithelial cells expressed the epithelial

264 logy of IL-33 and discussed the roles of the IL-33 in regulating airway immune responses and allergic

265 Genetic deletion of the IL-33 receptor paradoxically increases TSLP production,

266 We sought to study the role of the IL-33 receptor suppressor of tumorigenicity 2 (ST2) in t

267 Deletion of ST2, the IL-33 receptor alpha chain, or treatment with a soluble

268 In this article, we show that the IL-33-induced cytokine production is only partly depende

269 s (TAMs) in promoting metastasis through the IL-33-ST2-dependent pathway in xenograft mouse models of

270 itical for Treg homeostasis, upregulates the IL-33 receptor (ST2) on CD4(+) T cells, thus we hypothes

271 hat RV stimulates CXCL-10 expression via the IL-33/ST2 signaling axis, and that TLR2 signaling limits

272 d mice were treated with neutralizing Abs to IL-33 or recombinant IL-33, IL-25, or TSLP.

273 ist after antibiotic therapy, contributes to IL-33 locally and associated with Gr + bacteria coloniza

274 When exposed to IL-33, Treg cells upregulated their expression of the ca

275 peated intratracheal exposure to SplD led to IL-33 and eotaxin production, eosinophilia, bronchial hy

276 erine ILC2s, suggesting that they respond to IL-33 in a manner similar to ILC2s in other organs.

277 rowth and cytokine expression in response to IL-33 and thymic stromal lymphopoietin in vitro.

278 ir capacity to expand locally in response to IL-33.

279 regulated in WT-derived ILC2s in response to IL-33.

280 such as thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 may drive the progression from atopic d

281 antigen through combined induction of TSLP, IL-33, and OX40 ligand and that this can lead to suscept

282 L-3 +/- anti-IgE were coincubated with TSLP, IL-33, or IL-25.

283 ls increased in the lungs of mice undergoing IL-33-dependent allergen-driven airway inflammation.

284 nate immune system activation during various IL-33 driven pathologic disorders.

285 regulation of the PGE2/IL-17A/IL-22 axis via IL-33 signaling during lung fungal exposure.

286 cular T cells, and regulatory T cells, where IL-33 influences the development of chronic airway infla

287 ly present the cytokine to IL-1RAcP, whereas IL-33 binds to ST2 in order to conformationally constrai

288 localized to the airway epithelium, whereas IL-33 was expressed in epithelial and subepithelial cell

289 es, including Egr2, Ccl1, and Fxyd6, whereas IL-33 stimulation induced 823 genes, including Ccl1, Egr

290 lial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angi

291 (ICOSL) antibodies and then challenged with IL-33 and assessed for airway hyperreactivity.

292 and peribronchial inflammation compared with IL-33 alone.

293 ssion, and IL-13 production as compared with IL-33-challenged WT ILC2s.

294 ponse genes Ccl1, Il3, and Il2 compared with IL-33-stimulated BMBs.

295 The synergistic effect of LTC4 with IL-33 was completely dependent upon CysLT1R, because Cys

296 ereas treatment of naive wild-type mice with IL-33 induces immunosuppression.

297 oduction from purified ILC2s stimulated with IL-33 and resulted in NFAT1 nuclear translocation.

298 of naive BALB/c mice and those treated with IL-33.

299 Both in vivo and in vitro treatment with IL-33 induced type 2 cytokine production in uterine ILC2

300 In recent years, IL-33 has been implicated in the pathogenesis of immune-