ライフサイエンスコーパス: IL-13

1 IL-13 also binds to IL-13Ralpha2, considered as either a

2 IL-13 decreased claudin-18 expression in primary human c

3 IL-13 induced the preferential recruitment and suppressi

4 IL-13 is profibrotic, and it is released in a higher amo

5 IL-13 levels were increased in airway epithelial cells,

6 IL-13 released from IL-13(+)Th2 cells then promotes the

7 IL-13-driven gene expression was evaluated in several hu

8 IL-13-mediated signalling is initiated by binding to IL-

9 IL-13-neutralising antibodies act by preventing IL-13 bi

10 IL-13-producing CD8(+) T cells have been implicated in t

11 allow the improved detection of IL-4, IL-10, IL-13 and IL-17A ex vivo.

12 erferon [IFN-gamma], interleukin 10 [IL-10], IL-13, IL-6, granulocyte-macrophage colony-stimulating f

13 ytokine qPCR analysis revealed IL-10, IL-12, IL-13, IL-23 and TGFbeta were elevated, these were not s

14 -10), IFN-gamma, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and

15 rferon-gamma, interleukin (IL)-10, IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8 and tumour necro

16 ronchial epithelial cells to interleukin-13 (IL-13).

17 nflammatory and barrier markers (keratin 16, IL-13, IL-22, CCL17, CCL18, PI3/elafin, S100As, and lori

18 ly, B cells altered the production of IL-17, IL-13, and IFN-gamma, supporting a role for B cells func

19 reveal a cellular mechanism by which IL-4(+)IL-13(+) invariant NKT cells are necessary for IL-4Ralph

20 activation, including interleukin 4 (IL-4), IL-13, and FIZZ1.

21 hil cationic protein (ECP), total IgE, IL-4, IL-13 and IL-31 in children with AD (n = 56) compared to

22 their switch from a T helper (Th-2; ie IL-4, IL-13) to Th-1 (ie IFN-gamma) cytokine profile.

23 posure of AT to Th2 cytokines, such as IL-4, IL-13, and GM-CSF, stimulates ATM proliferation, whereas

24 an M2 profile with increase in CCL22, IL-4, IL-13, and IL-10 in both NLFS and COPDs.

25 vels of the inflammatory markers IL-1, IL-4, IL-13, and thymic stromal lymphopoietin.

26 The effect of IL-4, IL-13, IFN-gamma, and TNF-alpha on mucosal permeability

27 s pro-inflammatory cytokines including IL-4, IL-13, IL-17 and TNF-alpha.

28 IL-4, IL-13, or chitin polarizes macrophages toward the M2, or

29 released histamine and marked levels of IL-4/IL-13 (10-fold) when cocultured with A549 EC and IL-3, w

30 ) significantly increased expression of IL-4/IL-13 (M2)-responsive genes in murine bone marrow-derive

31 w insights as to the role environmental IL-4/IL-13 and the HR play in peripheral tolerance and the de

32 nt to environmental (i.e., physiologic) IL-4/IL-13 in the regulation of peripheral tolerance and the

33 tive mAb for AD, dupilumab, targets the IL-4/IL-13 receptor and was approved in early 2017 in the Uni

34 Ns-CIT regulated Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory cytokines (IL-10) in the br

35 d tissue eosinophils and inflammation, IL-5, IL-13 and AHR.

36 ase of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymphoid cells (ILC2s

37 bserved between blood eosinophilia and IL-5, IL-13, and eosinophil-derived neurotoxin (EDN), which st

38 nophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE production.

39 2, and RORalpha; were able to produce IL-5, IL-13, and IL-4; and, accordingly, were characterized by

40 s (thymic stromal lymphopoietin, IL-4, IL-5, IL-13, and the itch-specific cytokine IL-31 and their re

41 This exacerbation includes increase of IL-5, IL-13, eotaxin and MCP-3; infiltration of eosinophils in

42 total IgE, and did not correlate with IL-5, IL-13, eotaxin, or EDN.

43 , Th9, Th17/Th22 polar cytokines (i.e. IL-5, IL-13, IL-9, IL-17, IL-22).

44 ice markedly boosted ILC2 expansion and IL-5/IL-13 generation in a CysLT2R-dependent manner.

45 Expansion of ILC2s and IL-5/IL-13 generation reflected CysLT2R-dependent production

46 uced IL-33-mediated production of TNF, IL-6, IL-13, and MCP-1 in a concentration-dependent manner.

47 cells, IL-33 induces the production of IL-6, IL-13, and TNF-alpha.

48 The levels of IL-8, IL-13 and eosinophilic cationic protein (ECP) were also

49 Lack of EGFR expression on T cells abrogated IL-13 expression in infected tissues and impaired host r

50 ion with an RGD-containing peptide abrogated IL-13-enhanced contraction, with no further effect from

51 f chymase to human bronchial rings abrogated IL-13-enhanced contraction, and this effect was not due

52 at the Th2 cytokines, not only IL-4 but also IL-13, are involved in cognitive functions by stimulatin

53 However, liver fibrosis, an IL-13-mediated pathological consequence of wound healing

54 Tralokinumab (CAT-354) is an IL-13-neutralising human IgG4 monoclonal antibody that h

55 s eosinophilic asthma was associated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL

56 the fibrosis-associated cytokines IL-10 and IL-13 and extracellular matrix genes fibronectin and ost

57 kin and production of IL-4, IL-5, IL-10, and IL-13 are suppressed.

58 e production of IFN-gamma, IL-17, IL-10, and IL-13, with reductions observed at higher doses.

59 icroenvironment (eotaxin-2, IL-5, IL-18, and IL-13) and increased signalling molecules that support t

60 oid cells (ILC2s) expressing IL-33Ralpha and IL-13 compared with WT animals.

61 it is not known whether endogenous IL-4 and IL-13 contribute to the maintenance of peripheral tolera

62 ha1 heteroreceptor (HR) serves both IL-4 and IL-13 cytokines, which are believed to function as anti-

63 IL-4 and IL-13 have been defined as anti-inflammatory cytokines t

64 T cells and the IL-4Ralpha ligands IL-4 and IL-13 in the development of allergen-specific TH2 respon

65 a molecule with relatedness to both IL-4 and IL-13 is present, termed IL-4/13.

66 These observations suggest that IL-4 and IL-13 likely operate through the HR and influence Th17 c

67 d against the IL-4Ralpha subunit of IL-4 and IL-13 receptors.

68 IL-4 and IL-13 reduced epithelial cell SCD1 expression.

69 ti-EW and IgE levels, and increased IL-4 and IL-13 secretion after MCT/EW challenge.

70 IL-4 and IL-13 significantly increased the expression of HDACs an

71 the lack of signaling by endogenous IL-4 and IL-13 through the HR influences the function of effector

72 duced chemotaxis and the release of IL-4 and IL-13 which was specifically inhibited by anti-IL-31RA a

73 bers and levels of their cytokines, IL-4 and IL-13, decreased barrier integrity in ALI cultures of HB

74 itis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as prostasin th

75 It blocks the signaling pathways of IL-4 and IL-13, key cytokines that drive type 2 inflammatory resp

76 ch the common cytokine receptor for IL-4 and IL-13, namely the IL-4Ralpha/IL-13Ralpha1 (13R) heterore

77 The cytokines, interleukin (IL)-4 and IL-13, released from T-helper type 2 (Th2) cells, drive

78 this immune response in mammals are IL-4 and IL-13.

79 ly responsive to its known ligands, IL-4 and IL-13.

80 ated with a decreased production of IL-4 and IL-13.

81 s well as the release of histamine, IL-4 and IL-13.

82 ing downstream of the receptors for IL-4 and IL-13.

83 road repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helminth infection

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

85 associated with increased GM-CSF, IL-4, and IL-13 cytokine secretion among Ag-stimulated low-affinit

86 aired in Morris water maze-trained IL-4- and IL-13-deficient mice.

87 C2-driven proinflammatory cytokines IL-5 and IL-13 both in vitro and in vivo.

88 cells and produce the TH2 cytokines IL-5 and IL-13 but lack antigen-specific receptors.

89 significantly with serum levels of IL-5 and IL-13 but not IL-4 in preterm infants.

90 orldwide is driven by the cytokines IL-5 and IL-13 coming from Th2 cells, type 2 innate lymphoid cell

91 that produced the type 2 cytokines IL-5 and IL-13 during liver inflammation.

92 ibited CD4 T cell proliferation and IL-5 and IL-13 expression in vitro, and IP deficiency diminished

93 elease of signature cytokines IL-4, IL-5 and IL-13 from cells of both the innate and adaptive immune

94 dentified as the major producers of IL-5 and IL-13 in response to IL-25.

95 ells and IL-13(+)CD4(+) T cells and IL-5 and IL-13 production by lymph node cells but had no effect o

96 urther, CysLTs directly potentiated IL-5 and IL-13 production from purified ILC2s stimulated with IL-

97 estored eosinophil influx and IL-4, IL-5 and IL-13 production in lung tissue, as well as TH2 cell act

98 innate lymphoid cell infiltration, IL-5 and IL-13 production, as well as IL-17A(+) CD4 T cells.

99 d TLR6, and TLR stimulation induced IL-5 and IL-13 production.

100 naling significantly inhibited lung IL-5 and IL-13 protein expression, and reduced the number of lung

101 esent a major innate cell source of IL-5 and IL-13 required for mounting atheroprotective immunity, w

102 f indomethacin on STAT6-independent IL-5 and IL-13 responses in vivo.

103 the mean fluorescence intensity of IL-5 and IL-13 staining.

104 lls expressed significantly greater IL-5 and IL-13 than did hematopoietic prostaglandin D synthase-ne

105 )-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-resp

106 n of IFN-gamma whereas it inhibited IL-5 and IL-13, demonstrating its direct effect on attenuating Th

107 production of the type 2 cytokines IL-5 and IL-13, from human tonsillar and blood ILC2s in response

108 hils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple fo

109 -driven, pro-inflammatory cytokines IL-5 and IL-13.

110 BALF % CD4(+) T cells that produce IL-5 and IL-13.

111 ype cytokines such as interleukin (IL)-5 and IL-13.

112 ased numbers of immunopathologic IL-5(+) and IL-13(+) ILC2 and IL-17A(+) ILC3 compared with RSV-infec

113 e primary source of interleukin 5 (IL-5) and IL-13 during type 2 (allergic) inflammation in the lung.

114 lammatory cytokines interleukin-5 (IL-5) and IL-13 in lung lavage fluid, decreased regulatory T cell-

115 CCL17), and the synthesis of IL-4, IL-5, and IL-13 by T cells, in the course of the mixed lymphocyte

116 , and elevated production of IL-4, IL-5, and IL-13 in Hox5-deficient T cells compared with wild-type

117 ived mice produced less IFN-gamma, IL-5, and IL-13 than wild-type cells.

118 f proinflammatory cytokines (IL-4, IL-5, and IL-13) and decreased goblet cell hyperplasia.

119 ng classical TH 2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate c

120 s mediated by TH2 cytokines (IL-4, IL-5, and IL-13).

121 ugh release of the cytokines IL-4, IL-5, and IL-13, resulting in increased airway eosinophils and muc

122 heir effect by production of IL-4, IL-5, and IL-13.

123 on, and reduced the number of lung IL-5- and IL-13-expressing ILC2s, as well as the mean fluorescence

124 mation, with an increase in mainly IL-5- and IL-13-producing but not IL-4-producing TH2 cells in the

125 In particular, IL-5- and IL-13-producing type 2 ILCs (ILC2s) have been implicated

126 lower frequencies of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th

127 wnstream of mTOR activation (IL-2, IL-6, and IL-13), whereas in late PVR vitreous, cytokines driving

128 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 have important roles in stimulating innate and ada

129 etion of the type 2 cytokines IL-5, IL-9 and IL-13 that was dependent on cell-intrinsic expression of

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

131 hich stimulates the emergence of IL-9(+) and IL-13(+) ILC2s and mast cells and leads to development o

132 ymic stromal lymphopoietin (TSLP), IL-9, and IL-13, but not IL-5, in bronchoalveolar lavage fluid.

133 nes (eg, transforming growth factor-beta and IL-13) and alterations in matrix remodeling proteins (eg

134 -gamma, transforming growth factor-beta, and IL-13 as potential upstream regulators of the serum prot

135 s, IL-13(+) type 2 innate lymphoid cells and IL-13(+)CD4(+) T cells and IL-5 and IL-13 production by

136 phoid cells (CD45(+)lin(-)CD25(+) cells) and IL-13(+) ILC2s, emergence of a TSLP receptor-positive IL

137 CLK1 and IL-25 expression in enterocytes and IL-13 expression in mesenchyme were diminished.

138 ed mice, tuft cells, IL-25 in epithelium and IL-13 in the mesenchyme were significantly reduced, but

139 paired proliferation, GATA-3 expression, and IL-13 production as compared with IL-33-challenged WT IL

140 h1 and Th2 signature cytokines IFN-gamma and IL-13, respectively, or the T regulatory transcription f

141 n and decreased interleukin (IL)-4, IL10 and IL-13 protein levels.

142 -13+ innate lymphoid cells type 2 (ILC2) and IL-13+ gammadelta T cells.

143 , mucus production, airway inflammation, and IL-13-induced gene expression.

144 hat lead to induction of activated MDSCs and IL-13(+) Th2 cells have not yet been identified.

145 myeloid-derived suppressor cells (MDSCs) and IL-13(+) Th2 cells.

146 sion of airway mucosal CCL26, periostin, and IL-13-IVS all facilitated segregation of subjects into t

147 inhibited focal adhesion phosphorylation and IL-13-enhanced contraction, with no additional effect fr

148 reg cells abolished these effects of SEA and IL-13 expression in OVA-specific T cells.

149 profibrotic cytokines, such as TNFalpha and IL-13, are essential for C. muridarum to induce tubal fi

150 Although anti-IL-13 reduced nTreg cell-mediated enhancement, it was in

151 e time of anti-interleukin (IL)-17A and anti-IL-13 antibody fragments in the lungs and to improve the

152 e residence time of the anti-IL-17A and anti-IL-13 Fab' fragments in the lungs but PEGylation was abl

153 site of delivery of the anti-IL-17A and anti-IL-13 Fab' fragments within the lungs had a major impact

154 ify patients as suitable candidates for anti-IL-13 treatment.

155 cement; conversely, anti-IL-17, but not anti-IL-13, attenuated the enhancement by iTreg cells.

156 benefited more from PEGylation than the anti-IL-13 Fab' did.

157 Overall, IL-33 augmented IL-13 secretion from basophils cotreated with IL-3, with

158 ry bacteria by 24 and 48 hours, with all but IL-13 returning to baseline by seven days.

159 ng through a CCL2-CCR2 chemokine axis and by IL-13 expressing innate lymphoid cells.

160 nergistically induced in epithelial cells by IL-13 and human rhinovirus.

161 al barrier function that is downregulated by IL-13 and that claudin-18 deficiency results in increase

162 e in repairing epithelial changes induced by IL-13.

163 tioned in an epigenetic hotspot regulated by IL-13, a TH2 cytokine with increased levels in patients

164 CC10-IL-13 Tg mice developed considerable pulmonary tissue re

165 wed significantly lower accumulation in CC10-IL-13 Tg lungs relative to the specific tracer.

166 and MMP-13 were significantly higher in CC10-IL-13 Tg lungs.

167 as significantly higher in the lungs of CC10-IL-13 Tg mice than wild-type animals.

168 transgenic (Club cell 10-kDa protein [CC10]-IL-13 Tg) mice and wild-type littermates were used in th

169 ization decreased percentages of CD3(+)CD4(+)IL-13(+) and CD3(+)CD4(+)IL-17(+) cells in MLNs and decr

170 ed to underlie IL-13 overproduction in CD8(+)IL-13(+) cells from patients with SSc.

171 We have shown that CD8(+)IL-13(+) cells play a critical role in cutaneous fibrosi

172 Increases in serum cytokines and chemokines (IL-13, IL-22, CCL17) were found in AD versus healthy ind

173 duce high levels of the profibrotic cytokine IL-13, which induces collagen production by normal and S

174 y cellular sources of the signature cytokine IL-13.

175 and decreased expression of the Th2 cytokine IL-13 and the leukotriene-synthesizing enzymes 5-lipoxyg

176 evels of cellular infiltrates and cytokines (IL-13, IL-22, and S100As) were similarly reduced only by

177 Expression of TH2 cytokines (IL-13 and IL-31) was similar to that seen in control sub

178 ely reduced the expression of TH2 cytokines (IL-13, IL-4 and IL-5).

179 5-dependent IL-6 and the p38-MK2/3-dependent IL-13 production.

180 ously demonstrated a role for T cell-derived IL-13 in mediating the induction of collagen in dermal f

181 LC2 frequency was associated with detectable IL-13 in the urine and correlated with the level of recr

182 We also detected IL-13(+)IFN-gamma(+)ILC2 ex vivo in intestinal samples f

183 nature T helper cytokines of either disease, IL-13 and IL-17.

184 Runx2 was up-regulated by 6.4-fold during IL-13-induced goblet cell differentiation of human bronc

185 ronchial eosinophilic inflammation, elevated IL-13 production, and severe lung histopathology in comp

186 In vitro, IL-17A enhanced IL-13-induced gene expression in asthma-relevant murine

187 gene expression was associated with enhanced IL-13-driven signal transducer and activator of transcri

188 choalveolar lavage lymphocytes, eosinophils, IL-13, IL-5, and eotaxin were reduced in ROCK2(+/-) vs.

189 effects of OVA on lymphocytes, eosinophils, IL-13, IL-5, and mucous hypersecretion to wild-type leve

190 cantly decreased the numbers of eosinophils, IL-13(+) type 2 innate lymphoid cells and IL-13(+)CD4(+)

191 of recruited M-MDSCs, which highly expressed IL-13 receptor alpha1.

192 , ILC2 were increased and potently expressed IL-13 in the presence of BCG or tumor cells.

193 rosis factor-alpha, epidermal growth factor, IL-13, IL-17, IL-1alpha, and inducible protein-10.

194 -specific CD4 T cells were then analyzed for IL-13 and IFN-gamma expression.

195 IL-13 released from IL-13(+)Th2 cells then promotes the production of DOX-MD

196 levels of key inflammatory mediators (e.g., IL-13, CCL17, IL23p19, CXCL10).

197 healthy volunteers also secreted IFN-gamma, IL-13, IL-22, and cytolytic molecules.

198 low cytometry was used to measure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD

199 tingly, Th22 cells also expressed granzymes, IL-13, and increased levels of Tbet.

200 ediated ILC2 activation, resulting in higher IL-13 expression levels and M2 macrophage expansion in a

201 re of tralokinumab Fab in complex with human IL-13 to 2 A resolution.

202 Moreover, these results underline the ILC2/IL-13 axis as a targetable pathway to curtail the M-MDSC

203 remission, the levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored.

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

205 like receptor B as a molecular checkpoint in IL-13-induced eosinophil accumulation and activation, wh

206 murine cells, the IL-17A-driven increase in IL-13-induced gene expression was associated with enhanc

207 pectedly, ST2 deletion caused a reduction in IL-13(+) CD4 T cells, forkhead box P3-positive regulator

208 d by mixed TH2 and TH17 responses, including IL-13(+)IL-17(+)CD4(+) double-producing effector T cells

209 e ILC210 are distinct from those that induce IL-13 production, and gene expression data indicate that

210 ow that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of th

211 SEA-activated Treg cells induced IL-13 but suppressed IFN-gamma expression in OVA-specifi

212 3 to bind to the IL-13 promoter and inducing IL-13 upregulation.

213 nistic insight into how IL-17A can influence IL-13-driven responses.

214 way epithelial cells, FP treatment inhibited IL-13-induced suppression of FOXa2 gene expression and u

215 Corticosteroid treatment inhibits IL-13-induced GCM of the airways in asthma, possibly thr

216 Compared with mice given intratracheal IL-13 alone, those exposed to IL-13 and IL-17A had augme

217 d conventional dendritic cells produced less IL-13 and CCL17 and had impaired expansion of ILC2 in da

218 of the IL-4 receptor (Il4ra) and its ligand IL-13 are elevated in AT of obese C57BL/6 mice.

219 CS1 and A20, signaling inhibitors that limit IL-13 and IL-5 production.

220 In obese mice, ozone increased lung IL-13+ innate lymphoid cells type 2 (ILC2) and IL-13+ ga

221 type 2 inflammation based on airway mucosal IL-13-driven gene expression and how this related to cli

222 sed gene), (2) periostin, or (3) a multigene IL-13 in vitro signature (IVS).

223 y composed of residues in helices D and A of IL-13.

224 cruited but do not persist in the absence of IL-13.

225 e sought to establish the molecular basis of IL-13 overproduction by CD8(+) T cells from patients wit

226 athophysiology by increasing the capacity of IL-13 to activate intracellular signaling pathways, such

227 nificantly less pronounced downregulation of IL-13 in response to RNase 7 compared to healthy control

228 The effect of IL-13 on claudin expression was determined in primary hu

229 drug treatment counteracting the effects of IL-13 on the epithelium, we conclude that further explor

230 her how tralokinumab inhibits the effects of IL-13, we determined the structure of tralokinumab Fab i

231 g pathway and consequently the expression of IL-13.

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

233 C miR-126a(+) exosomal-mediated induction of IL-13(+) Th2 cells and tumor angiogenesis.

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

235 tion of inflammatory cells and the levels of IL-13 and IL-4 in OVA-challenged airways.

236 tion was assessed by using in vivo models of IL-13-induced lung pathology and in vitro culture of mur

237 etermined that therapeutic neutralization of IL-13, during the period of IL-13Ralpha2 saturation was

238 mediates the production of IL-6, but not of IL-13, whereas the p38-Mapk-activated protein kinases 2/

239 n directly contribute to the pathogenesis of IL-13-driven pathology.

240 lial cells differentiated in the presence of IL-13.

241 olecular mechanisms underlying production of IL-13 and other type 2 cytokines by CD8(+) T cells remai

242 reased expression of GATA3 and production of IL-13 by Th2 cells both in vitro and in vivo.

243 cytokine TSLP, as well as the production of IL-13, IL-4, and IL-5 by T cells in the course of the ML

244 cells (MDSCs) mediated by ILC2 production of IL-13, improved GI tract barrier function, and a preserv

245 +) T cells in the meninges and production of IL-13, whereas neither Morris water maze-trained IL-4 no

246 cells mediate fibrosis via the secretion of IL-13.

247 roup 2 innate lymphoid cells are a source of IL-13, which promotes lung regeneration.

248 rthermore, we determined cellular sources of IL-13 and effects of genetic deletion of the key type 2

249 The effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene expressio

250 t to the exacerbating influence of IL-17A on IL-13-induced responses, coexposure to IL-13 inhibited I

251 lymphoid cells (ILC2s) and are dependent on IL-13 and the innate cytokine IL-25.

252 Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-13 togeth

253 IL-13 alone was not sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue r

254 4ra expression and susceptibility to IL-4 or IL-13 treatment depend on IL-6 signaling, which seems to

255 A expression of other Th2 cytokines (IL-4 or IL-13).

256 In addition, upon stimulation with IL-4 or IL-13, HR(-) ETPs expressing virally transduced HR also

257 Whereas Lyn knockdown increased the IL-4 or IL-13-induced MUC5AC transcript and protein levels in th

258 eiotropic, soluble cytokines such as IL-4 or IL-13.

259 16HBE, Lyn overexpression decreased IL-4- or IL-13-induced MUC5AC transcript and protein levels.

260 The addition of IL-4 and/or IL-13 totally rescued fusion capacity.

261 based on airway mucosal CCL26, periostin, or IL-13-IVS gene expression.

262 pressive axis by specifically blocking PGD2, IL-13 and NKp30 partially restores ILC2 and M-MDSC level

263 13-neutralising antibodies act by preventing IL-13 binding to IL-13Ralpha1, IL-4Ralpha and/or IL-13Ra

264 ng to IL-13 helices A and D, thus preventing IL-13 from interacting with IL-13Ralpha1 and IL-13Ralpha

265 analysis reveals that tralokinumab prevents IL-13 from binding to both IL-13Ralpha1 and IL-13Ralpha2

266 2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T ce

267 oximately 92 cluster member miR-19a promoted IL-13 and IL-5 production and inhibited expression of se

268 ROCK2 inhibitors reduced IL-13-induced release of eotaxin from airway smooth musc

269 in airway epithelium is sufficient to rescue IL-13-induced AHR, inflammation, and mucus production, a

270 -12/23p40, which, when neutralized, restored IL-13 production and improved lung recovery.

271 ic leukaemia, tumour-activated ILC2s secrete IL-13 to induce myeloid-derived suppressor cells and sup

272 Lung-specific IL-13 transgenic (Club cell 10-kDa protein [CC10]-IL-13

273 This suggests that targeting IL-13 may be therapeutically beneficial.

274 ssion, AD serum showed up-regulation of Th2 (IL-13, CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10), Th1

275 Morris water maze task, we demonstrate that IL-13-deficient mice are significantly impaired in worki

276 a mouse model, we tested the hypothesis that IL-13 drives the progression of radiation-induced pulmon

277 These findings show that IL-13 acts as a molecular bridge between IELs and ECs, a

278 Mechanistically, we showed that IL-13 is able to stimulate primary astrocytes to produce

279 These data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-depende

280 Knockdown of Runx2 attenuated the IL-13-induced differentiation/mucus production by 67%.

281 es 2/3 (MK2/3) signaling module mediates the IL-13, but not the IL-6, production.

282 demonstrates that tralokinumab prevents the IL-13 pharmacodynamic effect by binding to IL-13 helices

283 GATA-3, allowing more GATA-3 to bind to the IL-13 promoter and inducing IL-13 upregulation.

284 on analysis determined GATA-3 binding to the IL-13 promoter.

285 e IL-13 pharmacodynamic effect by binding to IL-13 helices A and D, thus preventing IL-13 from intera

286 7A on IL-13-induced responses, coexposure to IL-13 inhibited IL-17A-driven antimicrobial gene express

287 mechanisms whereby IL-17A can contribute to IL-13-driven pathology in asthmatic patients remain uncl

288 intratracheal IL-13 alone, those exposed to IL-13 and IL-17A had augmented airway hyperresponsivenes

289 or primary human epithelial cells exposed to IL-13, IL-17A, or both.

290 pable of controlling integrated responses to IL-13 and affecting the function of other cell types suc

291 e key features of the asthmatic responses to IL-13 in murine models.

292 lammation, and mucus-production responses to IL-13, whereas treatment with an aerosolized agonist wor

293 r Morris water maze-trained IL-4 nor trained IL-13-deficient mice were able to increase CD4(+) T cell

294 ed clearance of inhaled allergens triggering IL-13 production by multiple cell types in the airways p

295 GATA-3 activity, which we showed to underlie IL-13 overproduction in CD8(+)IL-13(+) cells from patien

296 nder Th2 conditions in vitro by upregulating IL-13 expression.

297 eloid-derived suppressor cells (M-MDSCs) via IL-13 secretion.

298 epair and promotes tubular cell survival via IL-13 receptor alpha2 (IL13Ralpha2)-mediated signaling.

299 and gene expression pathways associated with IL-13-induced goblet cell metaplasia.

300 in dermal fibroblasts and that blockade with IL-13 antibodies attenuates this increase.