ライフサイエンスコーパス: IL-4

1 IL-4 amplifies IgE- and histamine-induced VE dysfunction

2 IL-4 and IL-13 have been defined as anti-inflammatory cy

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

4 IL-4 and IL-13 significantly increased the expression of

5 IL-4 drives production of these structurally related def

6 IL-4 exacerbation of histamine-induced hypovolemic shock

7 IL-4 level was the highest, and Th17/Th2 levels were the

8 IL-4 promoted epithelial Wnt5a secretion, which upregula

9 IL-4 secretion by ILC2s contributes to the allergic resp

10 IL-4, IFN-gamma, and TNF-alpha enhanced mucosal permeabi

11 IL-4, IL-13, or chitin polarizes macrophages toward the

12 IL-4, TSLP, IL-17A, EPO activity, total cell count and s

13 IL-4- and histamine-induced ABL1 activation in human VE

14 IL-4-induced gene-1 (IL4I1), a secreted l-phenylalanine

15 (+)CRTh2(+) T-cell proliferation (P < 0.01), IL-4, and IL-5 levels (all P < 0.01).

16 est levels of the inflammatory markers IL-1, IL-4, IL-13, and thymic stromal lymphopoietin.

17 tokines (TNF-a, IL-3) but not others (MCP-1, IL-4).

18 travaginally infected wild-type, IL-10(-/-), IL-4(-/-), and IL-4Ralpha(-/-) mice with low-dose C. tra

19 al immunoglobulin (IgM) and cytokine (IL-10, IL-4) production, thus providing the possibility of the

20 , IL-8, interferon gamma-induced protein 10, IL-4, IL-9, IL-10, fibroblast growth factor 2, IL-7, IL-

21 E levels, increased IFN-gamma/IL-4 and IL-10/IL-4 ratios, DNA remethylation at the IL-4 promoter and

22 uced the expression of TH2 cytokines (IL-13, IL-4 and IL-5).

23 ne TSLP, as well as the production of IL-13, IL-4, and IL-5 by T cells in the course of the MLR, was

24 or quantification of interleukin (IL)-1beta, IL-4, IL-6, IL-17, and tumor necrosis factor-alpha using

25 nificantly higher levels of IL-10, IL-1beta, IL-4 and IL-2 in both MCI groups (P<0.001), while there

26 More recently, the type 2 IL-4 has been demonstrated to play a role in cognition.

27 stemic but not TB antigen-stimulated type 2 (IL-4 and IL-5) and regulatory (transforming growth facto

28 pathway that stabilizes interleukin-2(IL-2), IL-4, and IL-10 messenger RNA (mRNA) transcripts.

29 Plasma interleukin (IL) 2, IL-4, IL-5, IL-7, IL-17, interferon-gamma, and tumor nec

30 activated by the endogenous cytokines IL-2, IL-4, and IFN.

31 A stability and inhibited secretion of IL-2, IL-4, and IL-10.

32 in (IL)-10, IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8 and tumour necrosis factor-alpha.

33 erferon-gamma, interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, tumor necrosis factor-alpha, epidermal

34 nd cytokines examined (interleukin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma interferon [IFN-gamma]) a

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

36 transcription in response to interleukin 4 (IL-4), hence class switching to IgE and IgG1, is not ful

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

38 the phenotypic conversion of interleukin 4 (IL-4)-activated monocyte-derived F4/80(int)CD206(+)PD-L2

39 ype 2 cell signature cytokine interleukin-4 (IL-4) hampers neutrophil expansion and migration by anta

40 cells signaling triggering to interleukin-4 (IL-4) overexpression.

41 with exposure, with increased interleukin-4 (IL-4) production, IL-5 transcription, and eosinophilia.

42 tokines examined, Ag-specific interleukin-4 (IL-4) T-helper enzyme-linked immunosorbent spot (ELISpot

43 bset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses during helmint

44 ant protein A (SP-A) enhanced interleukin-4 (IL-4)-dependent macrophage proliferation and activation,

45 Interleukin-4 (IL-4)-induced T helper (Th) 2 cells promote susceptibili

46 Long-acting IL-4 complex (IL-4c; recombinant IL-4 mixed with anti-IL

47 Additionally, IL-4 was associated with a higher likelihood of severe A

48 ant for how polymorphisms in genes affecting IL-4 responses influence the risk of IgE-mediated allerg

49 STAT6 activation potencies observed for all IL-4 variants.

50 Although IL-4 promoted expression of the FcepsilonRIIb isoform on

51 vivo, and that genital administration of an IL-4-expressing adenoviral vector greatly increased in v

52 d increased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

53 flammatory cells and the levels of IL-13 and IL-4 in OVA-challenged airways.

54 alpha; were able to produce IL-5, IL-13, and IL-4; and, accordingly, were characterized by demethylat

55 Interleukin (IL)-1beta and IL-4 were independently associated with ASD compared wit

56 ated with lower levels of IL-1beta, IL-2 and IL-4 (P<0.05).

57 eta being most dominant followed by IL-6 and IL-4.

58 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in teleost fish.

59 induction by tumor necrosis factor-alpha and IL-4 was enhanced.

60 Monocytes integrated GM-CSF and IL-4 stimulation combinatorically and temporally, result

61 ed upon B-cell receptor (BCR) engagement and IL-4 treatment.

62 activation requires allergen re-exposure and IL-4 production by CD4 T cells.

63 ed with CM-MSC showed increases in FOXP3 and IL-4 expression and positively affected the Treg:Th17 ba

64 8(+) T cells and production of IFN-gamma and IL-4, in an Ag-independent manner.

65 isplay increased production of IFN-gamma and IL-4.

66 g to the Gata3 locus and decreased Gata3 and IL-4 expression, supporting a role for HOX5 proteins in

67 Half-maximal rates for histamine (4 h) and IL-4 (5 h) secretion were slower than observed with stan

68 responded to cold by releasing histamine and IL-4, and this medium stimulated UCP1 expression and lip

69 IL-3, with minimal effects on histamine and IL-4.

70 and correlate with IgE levels in humans, and IL-4 promotes IgE and IgG1 Ab production against allerge

71 ontrast to the eosinophilic inflammation and IL-4 production observed in allergic mice with HS.

72 tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE production.

73 sfer of ILC2s restored eosinophil influx and IL-4, IL-5 and IL-13 production in lung tissue, as well

74 , antigen-specific IgE, cytokine levels, and IL-4, INF-gamma and Foxp3 gene promoter DNA methylation

75 cyte CCL17 production in response to LPS and IL-4.

76 Ndfip1 restricts Treg cell metabolism and IL-4 production via distinct mechanisms, as IL-4 deficie

77 olutionarily conserved because early NKT and IL-4 gene signatures also positively correlate with the

78 Antagonizing IL-4 prevented mucosal barrier disruption and tight junc

79 lex (IL-4c; recombinant IL-4 mixed with anti-IL-4 monoclonal antibody as a stabilizer) was administer

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

81 ow, MPO downward arrow, CD68 downward arrow, IL-4 upward arrow, IL-10 upward arrow, and TGF-beta upwa

82 IL-4 production via distinct mechanisms, as IL-4 deficiency does not prevent hyperproliferation or e

83 encode immunosuppressive cytokines, such as IL-4 and IL-10.

84 ty of pleiotropic, soluble cytokines such as IL-4 or IL-13.

85 ion factors and output of cytokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

86 hat exposure of AT to Th2 cytokines, such as IL-4, IL-13, and GM-CSF, stimulates ATM proliferation, w

87 In male subjects with ASD, IL-4 was negatively associated with nonverbal cognitive

88 re likely to lose Foxp3 expression to become IL-4-producing TH2 effector cells.

89 be differentially expressed >3-fold between IL-4-stimulated wild-type and STAT6(-/-) B cells (75 upr

90 IL-13Ralpha1 heteroreceptor (HR) serves both IL-4 and IL-13 cytokines, which are believed to function

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

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

93 of IL-6 and IL-21, and to a lesser extent by IL-4 and TNF-alpha.

94 ulated and 149 were downregulated >3-fold by IL-4 in a STAT6-dependent manner.

95 , IL-5Ralpha, STAT5, and Thy1 are induced by IL-4 in a STAT6-dependent manner.

96 ng infection, but were locally maintained by IL-4 and IL-10.

97 1 phenotype and function can be modulated by IL-4.

98 Effects of omalizumab on IgE production by IL-4/anti-CD40-treated PBMCs from allergic patients were

99 cyte gene expression is critically shaped by IL-4, altering cell fate decisions, which are likely imp

100 Acute or chronic stimulation by IL-4 modified expression of more than 1000 genes express

101 ly activated form of STAT6 is able to bypass IL-4 upstream signalling and instruct dendritic-cell-spe

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

103 ckdown of miR-363 in CLL cells prior to CD40/IL-4 stimulation prevented the ability of CLL-EVs to ind

104 ction by B cells when stimulated with CD40L, IL-4, and IL-21 was also determined.

105 Moreover, rfhSP-D inhibited CD40L/IL-4- and IL-21-mediated IgE production (77.12%; P = 0.0

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

107 om monocytes cultured for 5 days with GM-CSF+IL-4 or isolated from peripheral blood (CD1c+ DC).

108 abetes was associated with increased GM-CSF, IL-4, and IL-13 cytokine secretion among Ag-stimulated l

109 crophage colony-stimulating factor [GM-CSF], IL-4, and MIP-1alpha) responses of the treated mice was

110 elopment, including the pleiotropic cytokine IL-4.

111 he expression of the TH2-polarizing cytokine IL-4 and the T-cell activation markers CD69 and CD62L.

112 Although the cytokine IL-4 is required for the development of IgE-producing pl

113 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from pat

114 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from pat

115 Eosinophils and their associated cytokines IL-4 and IL-5 are emerging as central orchestrators of t

116 erized by the release of signature cytokines IL-4, IL-5 and IL-13 from cells of both the innate and a

117 cytokines IL-2 and IL-12, and Th2 cytokines IL-4 and IL-10, particularly during the acute phase of i

118 of disease through release of the cytokines IL-4, IL-5, and IL-13, resulting in increased airway eos

119 ed signaling among classical TH 2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotax

120 reduced levels of proinflammatory cytokines (IL-4, IL-5, and IL-13) and decreased goblet cell hyperpl

121 ased mRNA expression of other Th2 cytokines (IL-4 or IL-13).

122 MNs-CIT regulated Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory cytokines (IL-

123 c inflammation is mediated by TH2 cytokines (IL-4, IL-5, and IL-13).

124 cell numbers and levels of their cytokines, IL-4 and IL-13, decreased barrier integrity in ALI cultu

125 y the colitis-associated Th2-type cytokines, IL-4 and IL-13, down-regulates matriptase as well as pro

126 ll line, 16HBE, Lyn overexpression decreased IL-4- or IL-13-induced MUC5AC transcript and protein lev

127 vivo, increasing IFN-gamma while decreasing IL-4, IL-10, and Foxp3 expression by CD4(+) T cells-effe

128 berrant tissue repair in mice with deficient IL-4 signaling, we found that IL-4Ralpha and STAT6 signa

129 ra on Foxp3(+) cells, we further demonstrate IL-4 is required for the development of ex-Foxp3 Th2 cel

130 we reveal a central role for B cell-derived IL-4 and IL-4Ralpha in the optimal induction of the susc

131 Additionally, Tfh cell-derived IL-4 was required to maintain the Th2 response in the me

132 nd Th2 cells through co-culture, Th2-derived IL-4 promoted IL-10 expression by Th1 cultures, reducing

133 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in tel

134 tified peanut-specific highly differentiated IL-4(+) IL-5(+) Th2 cells.

135 Two tandem duplicated but divergent IL-4/13 A isoforms and one IL-4/13B are present, a uniqu

136 xpressing cell type in the heart during EAM, IL-4(-/-) mice were protected from DCMi like DeltadblGAT

137 Elevated IL-4 was associated with increased odds of severe ASD (o

138 whether the lack of signaling by endogenous IL-4 and IL-13 through the HR influences the function of

139 However, it is not known whether endogenous IL-4 and IL-13 contribute to the maintenance of peripher

140 Addition of omalizumab did not enhance IL-4/anti-CD40-induced IgE production in vitro.

141 An ERalpha-specific agonist enhanced IL-4-induced M2 gene expression in macrophages from both

142 e implanted with estrogen exhibited enhanced IL-4-induced M2 gene expression compared with macrophage

143 our findings suggest that estrogen enhances IL-4-induced M2 gene expression and thereby contributes

144 al new insights as to the role environmental IL-4/IL-13 and the HR play in peripheral tolerance and t

145 ockade inhibited while addition of exogenous IL-4 to Th1 cultures enhanced IL-10 production.

146 SEA-activated Treg cells expressed IL-4, upregulated CD69, and downregulated CD62L.

147 , and increased bronchoalveolar lavage fluid IL-4 and IL-5, whereas adoptive transfer of wild-type CD

148 in T cells, although largely dispensable for IL-4 induction, is critical for IL-33-driven Th2 effecto

149 were diminished, suggesting a time-frame for IL-4 treatment to be effective.

150 ce in which the common cytokine receptor for IL-4 and IL-13, namely the IL-4Ralpha/IL-13Ralpha1 (13R)

151 ng signaling downstream of the receptors for IL-4 and IL-13.

152 Il4 gene locus is specifically relevant for IL-4-dependent IgE responses to allergens with the amoun

153 lation with IL-4, and conditioned media from IL-4-stimulated macrophages failed to induce expression

154 Furthermore, IL-4-stimulated macrophages from female mice exhibited m

155 n, we examined gamma interferon (IFN-gamma), IL-4, IL-5, and IL-17 production by lung lymphocytes in

156 and ROR-gammat and production of IFN-gamma, IL-4 and IL-17, respectively.

157 increased specific production of IFN-gamma, IL-4, and IL-10.

158 CXCL1 (GROalpha), CXCL10 (IP-10), IFN-gamma, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF

159 istamine and IgE levels, increased IFN-gamma/IL-4 and IL-10/IL-4 ratios, DNA remethylation at the IL-

160 ns of Th1/2 lineage commitment genes (GATA3, IL-4, IL-4R, STAT4 and TBET) in umbilical cord DNA at bi

161 amydia was comparably cleared in all groups, IL-4(-/-) and IL-4Ralpha(-/-) mice displayed endometrial

162 ed a skewed Th2-type secretion profile (high IL-4/IFN-gamma ratio).

163 Interleukin-4 high (IL-4(hi)) FL-TFH cells, unlike FL B cells themselves, tr

164 Gata3-tg mice had lower IFN-gamma and higher IL-4 production with increased anti-viral IgG1 responses

165 n numbers and frequency but expressed higher IL-4 levels than those from nonatopic subjects.

166 CD203c as well as the release of histamine, IL-4 and IL-13.

167 together with birch pollen extract and human IL-4.

168 ther functional analysis of newly identified IL-4-regulated proteins in B cells that may contribute t

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

170 Instead, a combined deficiency in IL-4 and IL-10 was required to reverse the negative effe

171 DBA/1 mice doubly deficient in IL-4 and IL-10 were used to confirm that these two cytok

172 resulted in a modest but detectable drop in IL-4 production by CD4(+) T cells isolated from lymph no

173 NA sequencing to reveal the heterogeneity in IL-4-induced I transcription.

174 A corresponding increase in IL-4 and decrease in IFN-gamma and IL-17-expressing CD4(

175 Polymorphisms in genes involved in IL-4 responses segregate with allergic disease risk and

176 he lungs, while minimal changes were seen in IL-4- and IL-5-positive cells.

177 umerous pro-inflammatory cytokines including IL-4, IL-13, IL-17 and TNF-alpha.

178 ng culture with various cytokines, including IL-4 and TGF-beta1, suggesting that differentiation can

179 m IgG1 anti-EW and IgE levels, and increased IL-4 and IL-13 secretion after MCT/EW challenge.

180 ells exhibited decreased IL-10 and increased IL-4 expression in vivo and in vitro.

181 alpha-responsive B cells displayed increased IL-4 production as early as day 1 after infection.

182 (CpG)-induced IL-12p40 and allergen-induced IL-4 responses were associated with atopy.

183 w that during intestinal helminth infection, IL-4 derived from Tfh cells is required for IgE class sw

184 Interestingly, IL-4 treatment of bone marrow-derived macrophages (BMDMs

185 transcription factor GATA3 and intracellular IL-4 in bronchoalveolar lavage fluid T cells, but expres

186 unctionally responsive to its known ligands, IL-4 and IL-13.

187 ould be therapeutically manipulated to limit IL-4-induced IRS-2 signaling and polarization of M2 macr

188 TH2 cytokines (thymic stromal lymphopoietin, IL-4, IL-5, IL-13, and the itch-specific cytokine IL-31

189 ne expression and STAT6 phosphorylation in M(IL-4) cells.

190 porter mice showed eosinophils were the main IL-4-producing endometrial leukocyte (constitutively and

191 This was mainly IL-4 dependent.

192 xperiments showed eosinophils were the major IL-4-expressing cell type in the heart during EAM, IL-4(

193 that IL-4Ralpha and STAT6 signaling mediated IL-4-induced endometrial stromal cell (ESC) proliferatio

194 s is complex due to the presence of multiple IL-4/13 isoforms with overlapping but distinct activitie

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

196 in mainly IL-5- and IL-13-producing but not IL-4-producing TH2 cells in the lung.

197 a mansoni Here, we report that abrogation of IL-4 receptor alpha (IL-4Ralpha) signaling on B cells in

198 term activated in the presence or absence of IL-4 and analyzed for expression of >300 cell-surface pr

199 ltured for 4 d in the presence or absence of IL-4.

200 Addition of IL-4 also reduced the encephalitogenic capacity of Th1 c

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

202 Administration of IL-4 is known to augment M2 macrophages.

203 gE responses to allergens with the amount of IL-4 produced in the hemizygous condition falling close

204 Functional assessment of IL-4 expression was also performed.

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

206 We observed the development of IL-4-producing TFH cells and TH2 cells in draining lymph

207 ing T cells led to further downregulation of IL-4 and GATA3 expression, suggesting miR-24-mediated in

208 ion of the JAK3-STAT6 pathway, downstream of IL-4, is required for the acquisition of the dendritic-c

209 We explored the effect of IL-4 on the natural phenomenon of IL-10 production by a

210 The effect of IL-4, IL-13, IFN-gamma, and TNF-alpha on mucosal permeab

211 tle is known regarding the direct effects of IL-4 on keratinocyte function.

212 The effects of IL-4/ll-13 may be context dependent, with differing role

213 ta represent proof-of-concept of efficacy of IL-4 treatment for acute myocardial infarction, encourag

214 (MEKi) significantly increased expression of IL-4/IL-13 (M2)-responsive genes in murine bone marrow-d

215 0 surface proteins enabled identification of IL-4-upregulated surface proteins, such as CD90, CD108,

216 ugh Notch signaling and Gata3 independent of IL-4.

217 to dexamethasone, whereas the inhibition of IL-4 signaling could increase GC-induced apoptosis in re

218 Intravitreal injection of IL-4 and IL-10 ameliorated RPE toxicity that was induced

219 2 R-deficient mice secreted higher levels of IL-4, IL-5, and GM-CSF.

220 beta-HSD1 deficiency though plasma levels of IL-4, IL-6 and TNF-alpha were slightly affected by 11bet

221 lls) released histamine and marked levels of IL-4/IL-13 (10-fold) when cocultured with A549 EC and IL

222 It blocks the signaling pathways of IL-4 and IL-13, key cytokines that drive type 2 inflamma

223 overnight culture, especially in presence of IL-4, renders DCs responsive to both TSLP and IL-7.

224 signals required for the in vivo priming of IL-4-producing T cells are unknown.

225 lper (Tfh) cells are the primary producer of IL-4 in the reactive lymph node during type 2 immune res

226 as associated with a decreased production of IL-4 and IL-13.

227 in eosinophil levels and their production of IL-4 in the white and brown adipose tissues.

228 IPF patients and enhanced the production of IL-4, IL-17, and TGF-beta1 by these lymphocytes in contr

229 Gata3 expression, and elevated production of IL-4, IL-5, and IL-13 in Hox5-deficient T cells compared

230 phils exerting their effect by production of IL-4, IL-5, and IL-13.

231 gression to DCMi through their production of IL-4.

232 3a-5p is a post-transcriptional regulator of IL-4 expression and could have a role in IgE-mediated CM

233 IL-31 induced chemotaxis and the release of IL-4 and IL-13 which was specifically inhibited by anti-

234 to define the interaction and requirement of IL-4 and vascular endothelial (VE) IL-4 receptor alpha c

235 and by preventing pathological secretion of IL-4 from Treg cells.

236 of IgE-producing plasma cells, the source of IL-4 and cellular requirements for optimal IgE responses

237 lergens likely involve 2 distinct subsets of IL-4-producing CD4(+) T cells, namely TFH and Th2 cells.

238 y directed against the IL-4Ralpha subunit of IL-4 and IL-13 receptors.

239 lated chemokine/CCL17), and the synthesis of IL-4, IL-5, and IL-13 by T cells, in the course of the m

240 hibitor showed a significant upregulation of IL-4 mRNA and its protein expression.

241 Indeed, NKT cells secrete an early wave of IL-4 and constitute up to 70% of the total IL-4-producin

242 ta support a model wherein a pre-TfH wave of IL-4 secreted by interfollicular NKT cells triggers the

243 e FcepsilonRIIa isoform was not dependent on IL-4.

244 ted but divergent IL-4/13 A isoforms and one IL-4/13B are present, a unique situation compared to oth

245 ly suggests that the Th2 cytokines, not only IL-4 but also IL-13, are involved in cognitive functions

246 aRIIB following stimulation with IFNgamma or IL-4, respectively.

247 Different IL-4/13 paralogues (IL-4/13 A and IL-4/13B) exist in teleost fish.

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

249 These cells produced IL-4 and IL-21, and they more robustly promoted peanut-s

250 Long-acting IL-4 complex (IL-4c; recombinant IL-4 mixed with anti-IL-4 monoclonal antibody as a stabi

251 Together, our studies reveal IL-4-producing eosinophils stimulate ESC proliferation a

252 body temperature, behavioral effects, serum IL-4, IgE, and anti-drug Ab levels.

253 DeltadblGATA1 mice, and eosinophil-specific IL-4 deletion resulted in improved heart function.

254 ss to both IL-4 and IL-13 is present, termed IL-4/13.

255 is critical for TSLP responsiveness and that IL-4 can upregulate IL-7Ralpha on DCs.

256 Furthermore, we demonstrate that IL-4 and IL-33 promote up-regulation of PPARgamma in lun

257 These data demonstrate that IL-4 contributes to IL-10 production and that Th2 cells

258 Together, these results demonstrate that IL-4-producing and IL-4Ralpha-responsive B cells are cri

259 In vivo, we found that IL-4 has a differential regulatory role on expression of

260 We found that IL-4-stimulated bone marrow-derived and alveolar macroph

261 hemical inhibitors, we demonstrate here that IL-4-dependent Cox-1 up-regulation occurs at the post-tr

262 Collectively, our results indicate that IL-4-producing Tfh cells are central orchestrators of th

263 Here we show that IL-4 or IL-13 alone was not sufficient, but IL-4 or IL-1

264 These observations suggest that IL-4 and IL-13 likely operate through the HR and influen

265 Among the IL-4-induced changes, repression of fibronectin critical

266 IL-10/IL-4 ratios, DNA remethylation at the IL-4 promoter and demethylation at IFN-gamma and Foxp3 p

267 erous sclerosis complex-2 (Tsc2) blocked the IL-4-dependent expression of Cox-1 and the ability of ma

268 These data identified the IL-4/CXCL12 loop as a previously unrecognized pathway in

269 Whereas Lyn knockdown increased the IL-4 or IL-13-induced MUC5AC transcript and protein leve

270 In line with this, gene expression of the IL-4 receptor (Il4ra) and its ligand IL-13 are elevated

271 ation, presumably due to upregulation of the IL-4 receptor alpha.

272 can induce expression and activation of the IL-4/IL-4Ralpha/GATA3 axis in vitro.

273 In this paper, we have focused on the IL-4/13 isoforms found in the European sea bass (Dicentr

274 effective mAb for AD, dupilumab, targets the IL-4/IL-13 receptor and was approved in early 2017 in th

275 other in-vitro studies supported that these IL-4-mediated effects were induced via M2-like macrophag

276 This IL-4/CXCL12 axis was amplified in activated lymphoid str

277 ge numbers, and mediate this process through IL-4.

278 proliferation of macrophages in response to IL-4 or M-CSF.

279 se mice exhibits an increased sensitivity to IL-4 stimulation, indicated by an increased phosphorylat

280 ntly, Il4ra expression and susceptibility to IL-4 or IL-13 treatment depend on IL-6 signaling, which

281 f IL-4 and constitute up to 70% of the total IL-4-producing cells during the initial stages of infect

282 3, whereas neither Morris water maze-trained IL-4 nor trained IL-13-deficient mice were able to incre

283 ch was impaired in Morris water maze-trained IL-4- and IL-13-deficient mice.

284 on of IL-7Ralpha depending on the cell type; IL-4 decreases IL-7Ralpha expression on CD4 T cells wher

285 rement of IL-4 and vascular endothelial (VE) IL-4 receptor alpha chain (IL-4Ralpha) signaling in hist

286 In vitro, IL-4 blockade inhibited while addition of exogenous IL-4

287 these findings suggest a new paradigm where IL-4-dependent up-regulation of Cox-1 expression may pla

288 onal study thus aimed to investigate whether IL-4 administration is useful for the treatment of myoca

289 lly, we reveal a cellular mechanism by which IL-4(+)IL-13(+) invariant NKT cells are necessary for IL

290 also demonstrates a novel mechanism in which IL-4-dependent regulation of Cox-1 involves the activati

291 nt, expression of CXCL12 was associated with IL-4 expression and signaling within the FL BM and LN ni

292 gE(+) cells, we cultured tonsil B cells with IL-4 and anti-CD40.

293 ymptom scores were inversely correlated with IL-4 DNA methylation levels (P<.0002) and positively cor

294 GC-sensitive cells cultured with IL-4 display an increased resistance to dexamethasone, w

295 en intestinal organoids were stimulated with IL-4, tuft cells and IL-25 were induced in both WT and R

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

297 t release NE in response to stimulation with IL-4, and conditioned media from IL-4-stimulated macroph

298 ntrol subjects, EoE associated strongly with IL-4/kinesin family member 3A (IL4/KIF3A) (P = 2.8 x 10(

299 Studies with IL-4-IRES-eGFP (4get) reporter mice showed eosinophils w

300 Furthermore, chronic treatment with IL-4 failed to increase energy expenditure in wild-type,