ライフサイエンスコーパス: IL-13

1 IL-13 and virus infection mediated effects on ACE2 expre

2 IL-13 has an important role in atopic dermatitis (AD) pa

3 IL-13 levels were associated with protection against pne

4 IL-13 modulates ACE2 and TMPRSS2 expression in airway ep

5 IL-13 significantly reduced ACE2 and increased TMPRSS2 e

6 IL-13 stimulation decreased miR-1 levels in human lung e

7 IL-13 stimulation of EPC2-air-liquid interface cells led

8 IL-13 suppressed IL-12 production by mouse skin-derived

9 IL-13 together with IL-4 failed to demonstrate any syner

10 IL-13 was necessary and sufficient for induction of CD11

11 IL-13-CD38-cADPR-dependent SAP sampling of food allergen

12 C2s (P = .002) and IL-5(+) cells (P = .042), IL-13(+) cells (P = .042), and IL-5(+)IL-13(+) ILC2s (P

13 Plasma and BAL IL-4, IL-6, IL-10, IL-13 and TNF-alpha correlated with BAL fungal presence,

14 The cytokines IL-10, IL-13, IL-4, and IL-1alpha were negatively associated wi

15 1beta, IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TN

16 The anti-interleukin 13 (IL-13) monoclonal antibody lebrikizumab improves lung fu

17 terized by the production of interleukin 13 (IL-13), which drives expulsion.

18 sed interleukin 5 (IL-5) and interleukin 13 (IL-13)] and T regulatory type-1 (Tr1) (IL-10) response w

19 itical up-stream mediator of interleukin-13 (IL-13) and IL-4 signaling and is constitutively activate

20 und that the type 2 cytokine interleukin-13 (IL-13) is induced in exercising muscle, where it orchest

21 gests that activation of the IL-4-HIF-1alpha-IL-13 axis might play a role in the development of stero

22 ificantly more interleukin 1beta (IL-1beta), IL-13, IL-17, IL-22, and KC, and showed severe immune ce

23 Our results identified TNF-alpha, IL-1beta, IL-13, IFN-gamma and LPS as robust in vitro stimuli of c

24 higher serum IgG1 and IgE levels, more IL-4, IL-13 mRNA expression in OVA-sensitized skin, and lower

25 on by IFN-gamma, IFN-beta, IFN-lambda, IL-4, IL-13, and IL-10 cytokines to better understand the hete

26 ater for interferon gamma (IFN-gamma), IL-4, IL-13, and IL-10.

27 , type 2 innate lymphoid cells, IL-33, IL-4, IL-13, and mucus) that directly hinders larval developme

28 m autocrine/paracrine IL-10, TGF-beta, IL-4, IL-13, IL-22, and TSLP secretion and SOCS1/SOCS2/SOCS3 i

29 Levels of IL-4, IL-13, IL-33, and IL-1beta were significantly higher in

30 ism of IL-4Ralpha signaling suppresses IL-4-/IL-13-dependent processes, such as mucosal IgE formation

31 ed receptor component for interleukin (IL)-4/IL-13, key drivers of type 2 inflammation.

32 gene expression in ECs challenged with IL-4/IL-13 and house dust mite (HDM) extract.

33 , transcripts of neutrophils exposed to IL-4/IL-13 and monocyte responses to IFN-gamma or IFN-beta em

34 Notably, only dual IL-4/IL-13 blockade prevented eosinophil infiltration into lu

35 rapeutic mechanism of dupilumab, a dual IL-4/IL-13 blocker, in multiple type 2 diseases.

36 ned genetic suppression of hepcidin and IL-4/IL-13 in macrophages failed to improve cardiac function

37 either IL-4 or IL-13 inhibition to dual IL-4/IL-13 inhibition, we demonstrate that blockade of both I

38 Ralpha(-/lox)) and mice lacking IL-4 or IL-4/IL-13 on B cells were sensitized and challenged with hig

39 and regeneration through modulation of IL-4/IL-13 pathways.

40 , we have demonstrated that blockade of IL-4/IL-13 signaling aborted IgE production after activation

41 rleukin) -4 receptoralpha mAb, inhibits IL-4/IL-13 signaling and is indicated for the treatment of in

42 ontrolled AD, asthma and CRSwNP because IL-4/IL-13 signaling is a key driver of type2/Th2 immune dise

43 ckdown model to investigate the role of IL-4/IL-13 signaling prior to the onset of the disease and du

44 This is because IL-4/IL-13 signaling through the HR inhibits their T cell pot

45 osynthesis, glycolysis, and interleukin IL-4/IL-13 signaling.

46 IL-4R antagonist transiently inhibited IL-4/IL-13 signalling at the vaccination site.

47 s) were treated with M-CSF, followed by IL-4/IL-13 to induce the M2a allergic phenotype.

48 ruitment of eosinophils by secretion of IL-4/IL-13, which leads to STAT6-dependent expression of CCL2

49 own to facilitate basophil secretion of IL-4/IL-13, with implications that this unique mode of activa

50 In mice, Arg1 was upregulated in an IL-4/IL-13- and intestinal microbiota-dependent manner.

51 ed ear swelling was further observed in IL-4/IL-13-deficient and STAT6-deficient mice.

52 lux in immune control in the absence of IL-4/IL-13-dependent immune mechanisms.

53 IL-4/IL-13-induced STAT6 phosphorylation serves to enhance IR

54 gration toward CXCL8, thereby mirroring IL-4/IL-13-stimulated neutrophils.

55 .042), IL-13(+) cells (P = .042), and IL-5(+)IL-13(+) ILC2s (P = .003) compared with NACs.

56 ) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils.

57 erresponsiveness through production of IL-5, IL-13 and VEGFA.

58 TGFbeta1-mim downregulated IL-2, IL-4, IL-5, IL-13, and IFN-gamma, upregulated IL-10, and induced Tre

59 The type 2 cytokines IL-5, IL-13, and IL-4 play an important role in the induction

60 al application of equimolar amounts of IL-5, IL-13, and IL-4, alone or in combination.

61 s in pro-allergic cytokines, including IL-5, IL-13, and IL-9 and decreased basophil activation.

62 respectively, with 100 ng/mL of IL-4, IL-5, IL-13, or IL-17A, and contractile responses, Ca(2+) mobi

63 osinophilia, eotaxin-2 expression, IL-4/IL-5/IL-13 production, mucus production) in the airways and l

64 CRSwNP by profound elevations in IL-5, IL-6, IL-13, and IFN-gamma; however, significant heterogeneity

65 particularly cytokines, such as IL-4, IL-6, IL-13, IL-17A, or TNF-alpha, have substantially improved

66 reduced the production of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, with inhi

67 tometry was used to measure IFN-gamma, IL-9, IL-13, IL-17, and IL-22 cytokine levels in CD4(+)/CD8(+)

68 2s with E2 prior to IL-13 exposure abrogated IL-13-induced architectural changes and esophageal barri

69 n and rapid upregulation of expression after IL-13 stimulation, that ANO1 is the primary apical IL-13

70 lamina propria mucosal mast cells through an IL-13-CD38-cyclic adenosine diphosphate ribose (cADPR)-d

71 chemokine (P = 0.016), IgE (P = 0.023), and IL-13 (P = 0.031).

72 ammatory cytokine mRNA expression (IL-10 and IL-13).

73 ession of two major Th2 cytokines, IL-10 and IL-13.

74 s the p40 subunit of the cytokines IL-12 and IL-13 (ustekinumab), IL-17 (secukinumab, ixekizumab, bim

75 ene signatures induced in vitro by IL-17 and IL-13 in bronchial epithelial cells were used to identif

76 Finally, we found that IL-4 and IL-13 also inhibit the activity of Notch, a transcriptio

77 In addition, we found that IL-4 and IL-13 and Staphylococcus aureus lipoteichoic acid work i

78 mpact of the recombinantly produced IL-4 and IL-13 antagonist IL-4 mutein (IL-4M) on allergic sensiti

79 Interleukin (IL)-4 and IL-13 are both pivotal cytokines involved in the generat

80 Overall, these data support IL-4 and IL-13 as key drivers of type 2 inflammation and help pro

81 IL-4 and IL-13 blockade during experimental AIT demonstrates bene

82 human keratinocytes and suppressed IL-4 and IL-13 by 68%-83% (P < 0.05) in mast cells.

83 ll amounts of the related cytokines IL-4 and IL-13 by CD4(+) T cells isolated from the splenocytes of

84 to our knowledge, function by which IL-4 and IL-13 cytokines condition thymic microenvironment to rhe

85 We found that IL-4 and IL-13 engage a developmentally expressed IL-4Ralpha/IL-1

86 Consequently, ILC2-derived IL-4 and IL-13 feed back to induce eotaxin secretion from WAT-MSC

87 In mammals, IL-4 and IL-13 in concert with IL-10 are essential for balancing

88 Still, the role of IL-4 and IL-13 in neutrophil biology has not been well studied.

89 the redundant and distinct roles of IL-4 and IL-13 in type 2 inflammation and report dupilumab mechan

90 e demonstrate that blockade of both IL-4 and IL-13 is required to broadly block type 2 inflammation,

91 of the prototypic type 2 cytokines IL-4 and IL-13 on human neutrophils.

92 Exogenous IL-4 and IL-13 protect mice from antibody-mediated joint inflamma

93 Here, the effects of blockade of IL-4 and IL-13 signaling on different phases of AIT were addresse

94 nd type 2 (IL-4Ralpha/IL-13Ralpha1; IL-4 and IL-13 specific).

95 of proresolution type 2 cytokines (IL-4 and IL-13) dampens the proinflammatory effects of hypoxia th

96 creased levels of type-2 cytokines (IL-4 and IL-13) that repress keratinocyte (KC) differentiation.

97 lpha and inhibits signaling of both IL-4 and IL-13, has shown efficacy across multiple diseases with

98 nhibits signalling of interleukin (IL)-4 and IL-13, key drivers of type 2 inflammation, and has been

99 ly, biologics blocking TSLP, IL-33, IL-4 and IL-13, or IgE may help to achieve that.

100 e activation of T helper 2 cells by IL-4 and IL-13, the resolution of inflammation by IL-9, IL-5-indu

101 ncreased abundance of interleukin (IL)-4 and IL-13.

102 cells but not in cells treated with IL-4 and IL-13.

103 duction of T(H)2 cytokines, such as IL-4 and IL-13.

104 instrumental step in the release of IL-4 and IL-13.

105 for signaling following exposure to IL-4 and IL-13.

106 The Th2 cytokines interleukin 4 (IL-4) and IL-13 and the heterodimeric IL-4 receptor (IL-4R) comple

107 patients is induced by TH2 cells, IL-4, and IL-13 and HDAC activity.

108 of T cell cytokines such as IL-2, IL-4, and IL-13, which are produced by these cells upon in vitro s

109 -chain (IL-4Ralpha), essential for IL-4- and IL-13-induced STAT6 signaling.

110 Serum IL-5 and IL-13 decreased during climate treatment in asthma patie

111 (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate

112 y increased the numbers of ILC2 and IL-5 and IL-13 expression by ILC2 in the lung.

113 the number of lung ILC2 expressing IL-5 and IL-13 following Alt-Ext-challenge compared to WT mice.

114 ype 2 cytokines interleukin (IL)-4, IL-5 and IL-13 from T helper 2 (Th2) cells and innate lymphoid ce

115 Both challenges increased IL-5 and IL-13 in nasal fluids and serum and resulted in altered

116 MC produced a substantial amount of IL-5 and IL-13 in response to these flour extracts.

117 IL-5 and IL-13 markedly increased eosinophil numbers locally in l

118 are stimulated by IL-33 to increase IL-5 and IL-13 production and airway inflammation.

119 Tamoxifen decreased IL-5 and IL-13 production and BAL eosinophils.

120 IL-35 inhibited IL-5 and IL-13 production by ILC2s in the presence of IL-25 or IL

121 Lung ILC2, IL-5 and IL-13 production, and BAL inflammatory cells were measur

122 not Esr2(-/-) , mice had decreased IL-5 and IL-13 production, BAL eosinophils, and IL-33 release com

123 Prodigious levels of IL-5 and IL-13 were confined to HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T

124 We found that IL-5 and IL-13 were expressed not only by CRTH2(+) but also by CR

125 reduction in cytokine production of IL-5 and IL-13 while TGF-beta had no effect on ILC2 cytokine prod

126 ith elevations in type 2 cytokines (IL-5 and IL-13) and the type 1 cytokine, IFN-gamma.

127 tial and rapid source of IFN-gamma, IL-5 and IL-13, and IL-17A or IL-22, respectively.

128 sed the IL-25 receptor and produced IL-5 and IL-13.

129 d by increased interleukin (IL)-4, IL-5, and IL-13 in the OE.

130 ils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

131 hilia, protein level of lung IL-4, IL-5, and IL-13, and airway mucus score were also significantly de

132 y, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological mechanisms in asth

133 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13, which promote airway eosinophilia, mucus overprod

134 effector cytokines, such as IL-4, IL-5, and IL-13.

135 rototypical type 2 cytokines IL-4, IL-5, and IL-13.

136 tokine production, including IL-4, IL-5, and IL-13.

137 pe 2 cytokines Interleukin-(IL)-4, IL-5, and IL-13.

138 3 in mice reduced the production of IL-6 and IL-13 (two cytokines implicated in asthma) but not IL-5,

139 MK2/3 inhibition also suppressed IL-6 and IL-13 production by human ILC2s.

140 C1 inhibitor rapamycin also reduced IL-6 and IL-13 production, which would be consistent with a model

141 ith a model in which MK2/3 regulate IL-6 and IL-13 via mTORC1 activation in ILC2s.

142 -inflammatory cytokines (IFN-gamma, IL-6 and IL-13) in response to RSV compared to controls.

143 ced a range of cytokines, including IL-6 and IL-13.

144 rizing AAMPhi via mast cell-derived IL-6 and IL-13.

145 d had significantly lower levels of IL-6 and IL-13.

146 n-like growth factor-1, IFN-gamma, IL-6, and IL-13.

147 erferon-gamma, interleukin (IL)-6, IL-8, and IL-13, and lower monocyte chemokine, CCL2 (P < .01 for e

148 Last, SMs also increased IL-9 and IL-13 production and, under competing conditions, favore

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

150 s was followed by the appearance of IL-9 and IL-13, cytokines known for their roles in mast cell acti

151 eic T cell proliferation and IL-5, IL-9, and IL-13 production compared with native Ab-treated moDCs.

152 duction, followed by elevated IgE, IL-9, and IL-13 that maintain and enhance mast cell activation whi

153 c mRNA; increased numbers of eosinophils and IL-13-producing ILC2s; and exaggerated mucus metaplasia

154 n included IL-5 in addition to IFN-gamma and IL-13.

155 sed to identify patients with IL-17-high and IL-13-high asthma phenotypes.

156 ILC2s and IL-13 drove reciprocal ASC expansion and IL-33 expressio

157 xia (21% oxygen) or hypoxia (3% oxygen), and IL-13 production in vitro was monitored.

158 esses involved in cellular proliferation and IL-13-induced responses, and they highlight the importan

159 regulated IL13 expression in human skin, and IL-13 suppressed the capacity of LPS-stimulated human sk

160 trategies (e.g., Omega-6 supplementation and IL-13 inhibition for amyotrophic lateral sclerosis) and

161 all 256-fold affinity improvement of an anti-IL-13 antibody BAK1 as a result of InDel mutagenesis and

162 r aim was to determine whether RPC4046 (anti-IL-13 mAb) modulates EMT biomarkers in biopsy samples fr

163 stimulation, that ANO1 is the primary apical IL-13-induced Cl(-) transport mechanism within the esoph

164 Applying IL-13 increased ASL pH to ~7.4 without altering paracell

165 sponse of a key effector cytokine in asthma, IL-13.

166 E2 attenuated IL-13-induced architectural changes and esophageal epith

167 d with increased plasma and BAL IL-6 and BAL IL-13.

168 2 possesses a decoy function which can block IL-13 signaling.

169 ogic dupilumab prevented the effects of both IL-13 and IL-4 in human bronchi and human airway smooth

170 and bronchial hyperresponsiveness driven by IL-13.

171 iveness in isolated human airways induced by IL-13 and IL-4 provides further evidence that the IL-4Ra

172 otease, serine 2 (TMPRSS2), are modulated by IL-13.

173 xia-enhanced differentiation of T(C)2 cells, IL-13 production, and the capacity of transferred cells

174 In human airway smooth muscle cells, IL-13 and IL-4, but not IL-5 and IL-17A, enhanced the hi

175 medin U (NMU) supported IL-5 but constrained IL-13 expression and ILC2 proliferation.

176 DEP NK cells expressed GATA3 and cosecreted IL-13 and the killer protease granzyme B in response to

177 We hypothesized that PPIs can counteract IL-13-mediated esophageal epithelial responses that are

178 anulocyte colony stimulating factor (G.CSF), IL-13, IL-6, IL-12, interferon (IFN)-gamma, IFN-alpha, I

179 ng-resilient males showed the highest G-CSF, IL-13, and leptin levels.

180 A, and a profile of increased G-CSF, GM-CSF, IL-13, IL-6, IL-17a, leptin, and IL-4 that discriminated

181 e hypothesis that the pro-allergic cytokine, IL-13, can drive both corticosteroid-sensitive and corti

182 a robust response in inflammatory cytokines IL-13 and Il-17.

183 RK1/2 and P38), and production of cytokines (IL-13 and IL-6) following exposure to IgE/Ag were signif

184 Mast cell-derived IL-13 was required for induction of AAMPhi, whereas mast

185 ILC2-derived IL-13 was sufficient for RSV-driven AHR, since reconstit

186 MC-derived IL-13 acted on DCs from draining lymph nodes of OVA-sens

187 MC-derived IL-13 inhibited the T(H)1 cell response in contact hyper

188 n the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased pr

189 subjects when exogenous SP-A is added during IL-13 challenge.

190 y affected eosinophils but failed to enhance IL-13-driven effects on lung function or goblet cell met

191 fection also activates ILC2s chronically for IL-13 production and consequent asthma-like disease trai

192 trast, antagonism of the common receptor for IL-13 and IL-4 by the biologic dupilumab prevented the e

193 expression, demonstrating a requirement for IL-13 signaling in epithelial cells.

194 Clones proliferated and secreted IFN-gamma, IL-13 and cytolytic molecules following atabecestat or D

195 o measure levels of the cytokines IFN-gamma, IL-13, IL-9, IL-17, and IL-22 in CD4(+)/CD8(+) T cells i

196 unit (ICU) admission, whereas the IFN-gamma/IL-13 ratio and IL-10 levels were associated with an inc

197 ifferentiation in murine enteroids; however, IL-13, a cytokine induced by IL-33, markedly induces gob

198 of wild-type ILC2 rescued RSV-driven AHR in IL-13-deficient mice.

199 and exploratory outcomes included change in IL-13-associated biomarkers and measures of airway remod

200 Mice deficient in IL-13 showed decreased numbers of Tfh cells and germinal

201 um; and reduced surface P-selectin levels in IL-13-stimulated endothelial cells.

202 Our aim was to extend our work in IL-13 biology to determine whether airway epithelial cel

203 r participation in disease at all, including IL-13 production.

204 that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid def

205 er concentrations of biomarkers of increased IL-13 activity.

206 from IL-33-treated mice, IL-33 then induces IL-13 secretion by group 2 innate lymphoid cells and ent

207 ociated with STAT6 signaling, SP-A inhibited IL-13-induced STAT3 phosphorylation in mice and in human

208 ma phenotypes in murine models and inhibited IL-13-induced eosinophil binding to endothelial cells.

209 responsible for T. muris expulsion, inhibits IL-13 function both in vitro and in vivo.

210 Repeated HDM inhalation induced a mixed IL-13/IL-17A response and accumulation of IL-10-producin

211 p43 may open up new approaches to modulating IL-13 function and control of Trichuris infections.

212 By contrast, enhanced muscle IL-13 signaling was sufficient to increase running dista

213 In muscle, IL-13 acts through both its receptor IL-13Ralpha1 and th

214 b that potently and specifically neutralizes IL-13.

215 d with WT mice, we show that the activity of IL-13 is dramatically augmented in SP-A(-/-) mice, which

216 Blockade of IL-13-induced CD38/cADPR-dependent SAP antigen passaging

217 genously treated with SP-A in the context of IL-13 challenge.

218 as well as mice with selective deficiency of IL-13 in mast cells (MCs) were studied; in addition, den

219 t on ESR2 and associated with diminishing of IL-13-induced tyrosine kinase 2 and signal transducer an

220 features, with AD skin showing dominance of IL-13 pathways, but with near undetectable IL-4 expressi

221 se molecular pathways that are downstream of IL-13 and utilize the ERBB receptor and ligand family to

222 gic inhibition of RAGE blocks the effects of IL-13 and IL-4 by inhibiting sustained STAT6 activation

223 We determined effects of IL-13 treatment on ACE2 and TMPRSS2 expression ex vivo i

224 ss which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and

225 vage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-gamma mRNA (which i

226 ion on day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased num

227 These results reinforce the importance of IL-13 in airway pathobiology and suggest that neutraliza

228 but it also participates in the induction of IL-13 receptors and miR-126a expressed on/in the MDSCs.

229 cells, which is crucial for the induction of IL-13(+) Th2 cells, but it also participates in the indu

230 ctin and ST2/IL-1R4; and decreased levels of IL-13 and CD40 were found in all flavivirus group sample

231 d higher levels of IL-12 and lower levels of IL-13 than the recovered group.

232 lture medium for chronic disease modeling of IL-13-induced airway hyper-responsiveness.

233 ntegration of in vivo and in vitro models of IL-13-driven inflammation, we identify a role for the ep

234 chanism for SP-A in asthma as a modulator of IL-13-induced inflammation via mediating downstream IL-6

235 hobiology and suggest that neutralization of IL-13 may reduce asthmatic airway remodelling.

236 ficantly enhanced, with increased numbers of IL-13(+) T cells and increased production of IL-13 in vi

237 We report a rare population of IL-13-producing T(FH) cells present in mice and humans w

238 ith features consistent with the presence of IL-13 and EGFR/ERBB activation, with involvement of dist

239 ory response is suggested by the presence of IL-13, with infiltration of eosinophils and IgE-coated m

240 sulted in similar decreases in production of IL-13 and IL-9 by T cells, reduced mast cell accumulatio

241 IL-13(+) T cells and increased production of IL-13 in vitro.

242 Production of IL-13, IL-17A, and TNF-alpha was normal, but IFN-gamma p

243 died the transcriptional response profile of IL-13-exposed primary human airway epithelia in vitro an

244 Release of IL-13 by cutaneous MCs in response to mechanical skin in

245 his review provides an update on the role of IL-13 in AD and discusses the different strategies aimed

246 Our aim was to determine the role of IL-13 in initiation of the T(H) cell response to cutaneo

247 A higher secretion of IL-13 and IL-5 was detected in presence of the culprit d

248 t lung ILC2s that serve as a rapid source of IL-13 upon allergen exposure play a major role in Tfh ce

249 LC2s served as a predominant early source of IL-13 when naive mice were exposed to peanut flour.

250 tic manipulation of this endogenous brake on IL-13 signaling.

251 inal goblet cell hyperplasia is dependent on IL-13.

252 The effect of 17beta-estradiol (E2) on IL-13-induced signaling pathways, gene expression, and e

253 Dexamethasone had no effects on IL-13-induced hyperresponsiveness in human bronchi, the

254 etermined the effects of hypoxia exposure on IL-13-producing CD8(+) T(C)2 cells.

255 Only IL-13 was associated with airway eosinophilia, developme

256 Intranasal administration of either IL-4 or IL-13 confers an asthma-like phenotype in mice by induci

257 ptors, and their stimulation through IL-4 or IL-13 diminished their ability to form NETs and migrate

258 blood were assessed without or with IL-4 or IL-13 for (1) expression of IL-4 receptor subunits, (2)

259 ring in head-to-head studies, either IL-4 or IL-13 inhibition to dual IL-4/IL-13 inhibition, we demon

260 joints, and that CSF3 combined with IL-4 or IL-13 results in a prominent neutrophil up-regulation of

261 R1 and CXCR2 on human neutrophils on IL-4 or IL-13 stimulation in vitro.

262 produced IFN-gamma, but not IL-17, IL-4, or IL-13, and inhibited development of AHR through contact-

263 ly expressed Arg1 in response to IL-4 and/or IL-13, whereas skin or dLN fibroblasts failed to do so,

264 , nor did it solely block mucin synthesis or IL-13 receptor-proximal signaling.

265 , IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL11, G-CSF, GM-C

266 ta support the hypothesis that pharmacologic IL-13 inhibition ameliorates both inflammatory and remod

267 namycin and other HSP90 inhibitors prevented IL-13-induced goblet cell metaplasia in vitro and in viv

268 )13" cells have an unusual cytokine profile (IL-13(hi)IL-4(hi)IL-5(hi)IL-21(lo)) and coexpress the tr

269 lation of Th cells by IL-25 locally promoted IL-13 and IL-9 production.

270 lergen-specific IgE, inflammation, pulmonary IL-13 and airway hyper-responsiveness.

271 Recently, IL-13 has been suggested to be the key T2 cytokine drivi

272 N-gamma and IL-17A response to HDM, reducing IL-13 levels and airway eosinophilia without affecting I

273 D tissues showed preferential T(H)2 skewing (IL-13, CCL17/TARC, and CCL18), whereas psoriasis was cha

274 le, thereby providing evidence for targeting IL-13 in patients with AD.

275 ld lower fungal burden and with greater Th2 (IL-13) immune response.

276 We confirmed previous reports that IL-13 elicited modest induction of Ralpha2 in normal adu

277 Our data suggest that IL-13 may play a dual role in severe asthma: on the one

278 led across the SI epithelium mediated by the IL-13/CD38/cADPR pathway, regulate the onset of FIA reac

279 sequencing of isolated bronchi confirmed the IL-13-mediated upregulation of H(1) and CysLT(1) recepto

280 Furthermore, PPI treatment decreased the IL-13-induced proliferative response of esophageal epith

281 treatment reversed approximately 20% of the IL-13 transcriptome.

282 arrier dysfunction through inhibition of the IL-13/tyrosine kinase 2/signal transducer and activator

283 n on epithelial cells but indirectly through IL-13 production by goup 2 innate lymphoid cells.

284 ional responses of human esophageal cells to IL-13 and the PPIs omeprazole and esomeprazole were asse

285 IL-4 had similar, but weaker, effects to IL-13.

286 ranscriptome of airway cells when exposed to IL-13, but not when exposed to vehicle.

287 Binding of p43 to IL-13, the key effector cytokine responsible for T. muri

288 Pretreatment of EPC2s with E2 prior to IL-13 exposure abrogated IL-13-induced architectural cha

289 lls undergo transcriptional reprogramming to IL-13 production in the presence of IL-4 to become poten

290 d IL-6 enhanced macrophage responsiveness to IL-13 via upregulation of the IL-4Ralpha receptor.

291 were significantly altered in basal EV upon IL-13 treatment.

292 ust mite-induced asthma, we compared IL-4 vs IL-13 vs IL-4Ralpha blockers.

293 e inflammatory reaction underlying AD, where IL-13 is overexpressed locally and has a significant imp

294 uced inflammatory DC in the lungs along with IL-13 levels and overall inflammation.

295 icient and deficient in SP-A challenged with IL-13 and primary epithelial cells from participants wit

296 ctivated receptor 2 (PAR2) to cooperate with IL-13 in the induction of IL-25 in airway epithelial cel

297 h IL-17, and 9 patients were identified with IL-13 gene signatures.

298 source of p43 to facilitate interaction with IL-13, which may underpin chronic intestinal infection.

299 hil apoptosis in hypoxia, also observed with IL-13, required active STAT signaling, and was dependent

300 Treatment with IL-13 increased the potency of histamine, carbachol, and