ライフサイエンスコーパス: IL-4

1 IL-4 activated STAT6 signaling that, when silenced, sign

2 IL-4 activates macrophages to adopt distinct phenotypes

3 IL-4 activation of B cells is essential for class switch

4 IL-4 and IL-13 blockade during experimental AIT demonstr

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

6 IL-4 receptor alpha (IL-4Ralpha) is key in allergic asth

7 IL-4 receptor expression was detected in a variety of gl

8 IL-4 targets many cell types and induces multiple effect

9 IL-4 treatment improved long-term functional recovery in

10 IL-4 treatment markedly reduced the infiltration of CD8(

11 IL-4 treatment significantly reduced parasitemia, CM pat

12 IL-4, but not IL-5 or IL-17A, also increased the potency

13 IL-4-dependent, hypoxia-mediated increases in HIF-1alpha

14 IL-4-stimulated ILC2(10)s were isolated to evaluate cyto

15 proportions of IL-4(+) T(H)2 (V6, P = .02), IL-4(+) (V6, P = .003; V8, P = .004), and IL-21(+) (V6,

16 icited by IL-4, sequential delivery of MCP-1/IL-4 and coating components was distinct in young versus

17 aged mice, the sequential delivery of MCP-1/IL-4 was capable of restoring both recruitment and shift

18 ally, MCG increased anti-inflammatory IL-10, IL-4 and pro-angiogenic VEGF production, indicating a di

19 The cytokines IL-10, IL-13, IL-4, and IL-1alpha were negatively associated with tau

20 ecific) and type 2 (IL-4Ralpha/IL-13Ralpha1; IL-4 and IL-13 specific).

21 or alpha (TNF-alpha), IL-6, IL-12/23, IL-17, IL-4/13, IL-5, immunoglobulin E (IgE), integrins and B c

22 phine inhibited the expression of IL-1alpha, IL-4 and IL-17A.

23 -2, IL-12, interferon-gamma) and T-helper 2 (IL-4, IL-5) cytokines by 2 years of age were measured in

24 ) T cells that express interleukin-2 (IL-2), IL-4, and tumor necrosis factor alpha (TNF-alpha).

25 entrations of T cell cytokines such as IL-2, IL-4, and IL-13, which are produced by these cells upon

26 dependently of gp41, and inhibited the IL-2, IL-4, and IL-7 responses, as well as TCR-mediated activa

27 putative IL-10 elicitors revealed that IL-2, IL-4, IL-27, IL-10, and neuromedin U (NMU) increased IL-

28 on in mice, TGFbeta1-mim downregulated IL-2, IL-4, IL-5, IL-13, and IFN-gamma, upregulated IL-10, and

29 udies reporting on levels of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IF

30 The release of IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-10 and IL-17A from isolated, stimulated T

31 ells (Tfh) that produce interleukin (IL)-21, IL-4 and pathogenic cytokines, IL-17 and IFN gamma (IFNy

32 rental MSCs, including IL-1beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13, IL-17,

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

34 phages, type 2 innate lymphoid cells, IL-33, IL-4, IL-13, and mucus) that directly hinders larval dev

35 dherent eosinophils; and increases in IL-33, IL-4, IL-5, and IL-13 levels in lung tissue.

36 The Th2 cytokines interleukin 4 (IL-4) and IL-13 and the heterodimeric IL-4 receptor (IL-

37 nts, levels of Th2-associated interleukin-4 (IL-4) and IL-10 were also lower in miR155KO splenocyte s

38 Interleukin-4 (IL-4) is crucial in many helminth infections, but its ro

39 Although T(FH) cell-derived interleukin-4 (IL-4) is necessary for IgE production, it is not suffici

40 Interleukin-4 (IL-4) is produced by a unique subset of invariant natura

41 ecombinant viruses expressing interleukin-4 (IL-4) or interferon gamma (IFN-gamma) did not.

42 2) and CXCL8, without or with interleukin-4 (IL-4) pre-incubation.

43 Here, we report that interleukin-4 (IL-4) promotes oligodendrocyte regeneration and remyelin

44 ated microglia in response to interleukin-4 (IL-4) stimulation.

45 Interleukin-4 (IL-4) suppresses the development of multiple sclerosis i

46 nt on the T helper 2 cytokine interleukin-4 (IL-4), but not the T helper 1 cytokine interferon-gamma

47 cytokine activity, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological m

48 ociated with type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13, which promote airway eosinophili

49 beta 1 (TGF-beta1) because of interleukin-4 (IL-4)- and signal transducer and activator of transcirip

50 nd late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization.

51 ecently, we demonstrated that interleukin-4 (IL-4)-induced fusion of mouse macrophages depends on the

52 imulating factor (GM-CSF) and interleukin-4 (IL-4).

53 pendent on the T(H)2 cytokine interleukin-4 (IL-4).

54 anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected ear

55 Accordingly, IL-4 has been exploited as a therapeutic for several inf

56 After IL-4 treatment, the alternate pathway for pERK operates

57 lso exhibit increased STAT6 activation after IL-4 stimulation.

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

59 These results provide evidence of an IL-4-mediated pathology in Leishmania braziliensis-infec

60 els of IgE-mediated food allergy revealed an IL-4 signaling-dependent cell-intrinsic effect on SI MMC

61 TNF-alpha (P = 0.004), IL-2 (P = 0.004) and IL-4 (P = 0.009) median levels were elevated in PTB cult

62 nfidence interval, 0.29-0.82; P = 0.007) and IL-4 (odds ratio, 9.67; 95% confidence interval, 2.45-38

63 the M2a phenotype through elevated IL-10 and IL-4 expressing cells.

64 nt women with CL, interleukin-10 (IL-10) and IL-4 expression were approximately 3-times higher in les

65 tion of RAGE blocks the effects of IL-13 and IL-4 by inhibiting sustained STAT6 activation and downst

66 agonism of the common receptor for IL-13 and IL-4 by the biologic dupilumab prevented the effects of

67 umab prevented the effects of both IL-13 and IL-4 in human bronchi and human airway smooth muscle cel

68 isolated human airways induced by IL-13 and IL-4 provides further evidence that the IL-4Ralpha pathw

69 human airway smooth muscle cells, IL-13 and IL-4, but not IL-5 and IL-17A, enhanced the histamine-in

70 tream mediator of interleukin-13 (IL-13) and IL-4 signaling and is constitutively activated in malign

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

72 ion of equimolar amounts of IL-5, IL-13, and IL-4, alone or in combination.

73 We demonstrate that IL-4/13A and IL-4/13B are required for the maintenance of a Th2-like

74 n this study, we have generated IL-4/13A and IL-4/13B mutant zebrafish (Danio rerio) and, together wi

75 8 T cells producing IFN-gamma and IL-17- and IL-4-producing CD4 T cells that cannot mediate CHS.

76 enic OT-1 cells differentiated with IL-2 and IL-4 (T(C)2 cells) were exposed to normoxia (21% oxygen)

77 ro in response to interferon-gamma, IL-2 and IL-4 that is reverted by the JAK1/JAK2 inhibitor ruxolit

78 d distally in blood and BM, whereas IL-5 and IL-4 only increased eosinophils in lung and BM.

79 croglial phagocytic states, such as IL-6 and IL-4, and increased expression of microglial chemokines,

80 orylation downstream of RIG-I, IFN-beta, and IL-4, but not GM-CSF, signaling.

81 also enhanced expression of eNOS, CD31, and IL-4 with reduction of CCL28 and IL-6 levels associated

82 aive B cells upon stimulation with CD40L and IL-4 was similar in patients and controls, while patient

83 ncluding genes responding to both GM-CSF and IL-4, which had a higher centrality value in an antibody

84 tered on the ZBTB16 transcription factor and IL-4 signaling pathway is highly up-regulated due to E p

85 s, which produce the cytokines IFN-gamma and IL-4, respectively, displayed distinct patterns of DNase

86 responses to cytokines such as IFN-gamma and IL-4.

87 Finally, CSFs enhanced the IFN-gamma- and IL-4-induced polarization ability of AMs but not IMs.

88 combined genetic suppression of hepcidin and IL-4/IL-13 in macrophages failed to improve cardiac func

89 SF, GM-CSF, IL-13, IL-6, IL-17a, leptin, and IL-4 that discriminated between stress context (NOV > FA

90 inophil differentiation and recruitment, and IL-4, a major Th2 cytokine.

91 NKT cells, and enhanced IFN-gamma, TNF, and IL-4 production.

92 mbinantly produced IL-4 and IL-13 antagonist IL-4 mutein (IL-4M) on allergic sensitization and AIT ou

93 Here, we report on our use of anti-IL-4/13 monoclonal antibody (dupilumab) on two cases wit

94 ession of type 2 effector cytokines, such as IL-4, IL-5, and IL-13.

95 Plasma and BAL IL-4, IL-6, IL-10, IL-13 and TNF-alpha correlated with B

96 s of STIM1, but not STIM2, impaired basophil IL-4 production after stimulation with immunoglobulin E

97 ss of STIM2, but not STIM1, reduced basophil IL-4 production.

98 ely controlled AD, asthma and CRSwNP because IL-4/IL-13 signaling is a key driver of type2/Th2 immune

99 This is because IL-4/IL-13 signaling through the HR inhibits their T cel

100 ck from autocrine/paracrine IL-10, TGF-beta, IL-4, IL-13, IL-22, and TSLP secretion and SOCS1/SOCS2/S

101 Blocking IL-4 enhances IL-12 production by tumour-antigen-bearing

102 The peptides also boosted IL-4/GM-CSF induction of CD14, while only MVWGP and TGSY

103 a stimulated NFkappaB activation and boosted IL-4/GM-CSF induced expression of surface markers CD14 a

104 bition, we demonstrate that blockade of both IL-4 and IL-13 is required to broadly block type 2 infla

105 ds IL-4Ralpha and inhibits signaling of both IL-4 and IL-13, has shown efficacy across multiple disea

106 y an early decrease in the frequency of both IL-4+ cells and sIgE levels.

107 uction, but anti-PD-1 treatment reduced both IL-4 and TGF-beta production.

108 Thus, both IL-4/13 and IL-10 paralogs in zebrafish exhibit aspects

109 igated how alternative activation, driven by IL-4, modulated the phagosomal proteome to control macro

110 However, the response elicited by IL-4, sequential delivery of MCP-1/IL-4 and coating comp

111 generation of MMC9-like cells was induced by IL-4 and this was in part dependent on BATF.

112 ative polarization of macrophages induced by IL-4 is important for homeostasis and tissue repair.

113 on activated human Th cells is modulated by IL-4, and IL-3 regulates the effector functions of Th2 c

114 rferon-gamma and is controlled negatively by IL-4 signalling.

115 NFalpha-dependent, with TNFalpha produced by IL-4-polarized macrophages triggering MDA-MB-231 cell ap

116 0 gene transcripts reciprocally regulated by IL-4 signaling, including Il9 and Batf.

117 house dust mite-induced asthma, we compared IL-4 vs IL-13 vs IL-4Ralpha blockers.

118 ll receptor (TCR) stimulation for continuous IL-4 production in the steady state, since NKT2 cells lo

119 In contrast, IL-4 enhanced LPS tolerance, dampening proinflammatory r

120 to respond to the canonical type 2 cytokine IL-4, which underpins allergic disease and parasitic wor

121 and protein expression by the T(H)2 cytokine IL-4.

122 hway acted synergistically with the cytokine IL-4 by upregulating IL-2-STAT5 signaling and reducing i

123 driven by the prototypical type 2 cytokines IL-4, IL-5, and IL-13.

124 -2 more than the anti-inflammatory cytokines IL-4 and IL-10 in tonsil and blood samples in RAT, PTA,

125 5 and small amounts of the related cytokines IL-4 and IL-13 by CD4(+) T cells isolated from the splen

126 sed by increased levels of type-2 cytokines (IL-4 and IL-13) that repress keratinocyte (KC) different

127 and IFN-gamma) as compared to Th2 cytokines (IL-4 and IL-5) in splenocyte culture supernatants of the

128 rived MMC9 culture system was used to define IL-4-BATF signaling in MMC9 development.

129 Consequently, ILC2-derived IL-4 and IL-13 feed back to induce eotaxin secretion fro

130 th both tissue-resident and monocyte-derived IL-4-induced accessible regions but has different lineag

131 e therapeutic mechanism of dupilumab, a dual IL-4/IL-13 blocker, in multiple type 2 diseases.

132 Notably, only dual IL-4/IL-13 blockade prevented eosinophil infiltration in

133 ies, either IL-4 or IL-13 inhibition to dual IL-4/IL-13 inhibition, we demonstrate that blockade of b

134 Blockade of V-ATPase by archazolid during IL-4-induced human M2 polarization abrogated 15-lipoxyge

135 Intranasal administration of either IL-4 or IL-13 confers an asthma-like phenotype in mice b

136 by comparing in head-to-head studies, either IL-4 or IL-13 inhibition to dual IL-4/IL-13 inhibition,

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

138 We also quantified the effects of exogenous IL-4 on urothelial cell proliferation in vitro, includin

139 fferentiation 8)-positive T cells expressing IL-4 (Tc2) and reduced proportions of CD8(+) T cells exp

140 mmation (eosinophilia, eotaxin-2 expression, IL-4/IL-5/IL-13 production, mucus production) in the air

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

142 tion in vivo, whereas STIM2 was required for IL-4 production after combined IL-3 and IL-33 treatment

143 Downstream from IL-4 receptor signaling, STAT6 activation is transient,

144 days later for interferon gamma (IFN-gamma), IL-4, IL-13, and IL-10.

145 ed the vaccine efficacy with more IFN-gamma, IL-4, and CD8(+) memory T cells produced.

146 ereas other cytokines (eg, interferon-gamma, IL-4, and IL-10) were reduced.

147 e secretion, lowering the ratio of IFN-gamma:IL-4 production by NK1.1+ NKT cells.

148 IL-4R complexes: type 1 (IL-4Ralpha/gammac; IL-4 specific) and type 2 (IL-4Ralpha/IL-13Ralpha1; IL-4

149 In this study, we have generated IL-4/13A and IL-4/13B mutant zebrafish (Danio rerio) and

150 Hence, IL-4/IL13-targeting therapies prime the immune memory in

151 kin 4 (IL-4) and IL-13 and the heterodimeric IL-4 receptor (IL-4R) complexes that they interact with

152 s have an unusual cytokine profile (IL-13(hi)IL-4(hi)IL-5(hi)IL-21(lo)) and coexpress the transcripti

153 esults provide mechanistic insights into how IL-4 treatment mitigates experimental CM and have implic

154 lymph node and the development of IFNgamma, IL-4 and IL-17A responses without gain of other cytokine

155 Methods: Neutrophil activation of IL4Ra (IL-4 receptor alpha) signaling pathways was explored ex

156 the Th2 modulatory response was evaluated in IL-4 reporter mice.

157 Triggering of MSR1 in IL-4-activated macrophages leads to enhanced JNK activat

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

159 s in NOD-scid-Il2rg(-/-) mice was reduced in IL-4-stimulated human neutrophils compared with control

160 asia, and Th2 cytokine production, including IL-4, IL-5, and IL-13.

161 Mechanistically, IVIG induced IL-4 in human basophils by interacting with basophil sur

162 cy following disruption of anti-inflammatory IL-4/IL-10 polarization in vivo by transplantation of HS

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

164 (Interleukin) -4 receptoralpha mAb, inhibits IL-4/IL-13 signaling and is indicated for the treatment

165 ol biosynthesis, glycolysis, and interleukin IL-4/IL-13 signaling.

166 Intranasal IL-4 treatment warrants further investigation as a clini

167 ontrols (IL-4Ralpha(-/lox)) and mice lacking IL-4 or IL-4/IL-13 on B cells were sensitized and challe

168 mulation by IFN-gamma, IFN-beta, IFN-lambda, IL-4, IL-13, and IL-10 cytokines to better understand th

169 IL-35 inhibited CD40 ligand-, IL-4-, and IL-21-mediated IgE production by B cells (P =

170 tentiated by IL-21 in the context of limited IL-4.

171 activated, YY1(lo) NKT cells produced little IL-4 or IFN-gamma.

172 n in the steady state, since NKT2 cells lost IL-4 production when intrathymically transferred into CD

173 Further, eosinophilia, protein level of lung IL-4, IL-5, and IL-13, and airway mucus score were also

174 LPS/IFNgamma) or anti-inflammatory M2-like M(IL-4/IL-10) affected TNT-like protrusion formation, inte

175 In mammals, IL-4 and IL-13 in concert with IL-10 are essential for b

176 nd migration toward CXCL8, thereby mirroring IL-4/IL-13-stimulated neutrophils.

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

178 stead of mouse FcepsilonRIalpha and a mutant IL-4 receptor that lacks inhibitory function.

179 Targeting V-ATPase in M2 influenced neither IL-4-triggered JAK/STAT6 nor the mTOR complex 1 signalin

180 BALB/c mice and elicited IFN-gamma, but not IL-4 and IL-10, responses.

181 o ASCs in the setting of IFN-gamma-, but not IL-4-, induced inflammatory responses.

182 Using histocytometry, we observed IL-4-producing NKT2 cells localized to the thymic medull

183 l influx in immune control in the absence of IL-4/IL-13-dependent immune mechanisms.

184 PBMCs, we have demonstrated that blockade of IL-4/IL-13 signaling aborted IgE production after activa

185 While single delivery of IL-4 did not counteract the high inflammatory response o

186 Intranasal delivery of IL-4 nanoparticles after ICH hastened STAT6 activation a

187 The therapeutic effect of IL-4 is mediated through multiple mechanisms, including

188 e, we discovered a direct salutary effect of IL-4 on oligodendrocyte differentiation that was mediate

189 ST2 KO diminished the beneficial effects of IL-4 after ICH.

190 fferences were detected in the expression of IL-4 and TGF-1, while IL-10-expressing cells were lower

191 Expression of IL-4, but not IFN-gamma or IL-10, was positively correla

192 Arginine scarcity also dampens generation of IL-4 induced MGCs.

193 tively, these data confirm the importance of IL-4/STAT6/ST2 signaling in hematoma resolution and func

194 Time-dependent induction of IL-4, IL-21, and IL-6 was observed in nasal mucosa follo

195 veolar lavage fluid released lower levels of IL-4 and IL-5, and these results were paralleled by decr

196 CL2, CCL3, and CCL4, but decreased levels of IL-4, CXCL9, and CXCL10 compared to tumors from WT mice.

197 Levels of IL-4, IL-13, IL-33, and IL-1beta were significantly high

198 nd 1 day(s), respectively, with 100 ng/mL of IL-4, IL-5, IL-13, or IL-17A, and contractile responses,

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

200 We investigated the therapeutic potential of IL-4 against fatal malaria in Plasmodium berghei ANKA-in

201 mming to IL-13 production in the presence of IL-4 to become potent, steroid-insensitive, pathogenic e

202 nse against peanut, leading to production of IL-4 and IgE, but only the CC027/GeniUnc mice reacted to

203 he expression of C-MAF and the production of IL-4 and IL-10.

204 have differential roles in the production of IL-4, which are stimulus dependent.

205 ssociated with a reduction in proportions of IL-4(+) T(H)2 (V6, P = .02), IL-4(+) (V6, P = .003; V8,

206 ts were performed to test the requirement of IL-4 receptor alpha (IL-4Ralpha) signaling on MMC9s in e

207 Still, the role of IL-4 and IL-13 in neutrophil biology has not been well s

208 r findings reveal a new regenerative role of IL-4 in the central nervous system (CNS), which lies bey

209 stage malaria are largely known, the role of IL-4 remains less understood.

210 a knockdown model to investigate the role of IL-4/IL-13 signaling prior to the onset of the disease a

211 lysis of the redundant and distinct roles of IL-4 and IL-13 in type 2 inflammation and report dupilum

212 enhanced expression of CD69 and secretion of IL-4, IL-6, and IL-8.

213 Main sources of IL-4 and IL-10 were CD4+ and CD68+ cells, respectively.

214 EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable

215 Human neutrophils expressed both types of IL-4 receptors, and their stimulation through IL-4 or IL

216 tosomiasis by injecting the bladder walls of IL-4 receptor-alpha knockout (Il4ra(-/-) ) and wild-type

217 tors CXCR1 and CXCR2 on human neutrophils on IL-4 or IL-13 stimulation in vitro.

218 (IL-4Ralpha(-/lox)) and mice lacking IL-4 or IL-4/IL-13 on B cells were sensitized and challenged wit

219 lipopolysaccharide (LPS) pro-inflammatory or IL-4 anti-inflammatory stimulation revealed the importan

220 Adoptive transfer of TSG6- or IL-4-primed BMM s i.t.

221 TSG6- or IL-4-primed BMM s induced efferocytosis of apoptotic PMN

222 CD4(+) T cells in response to TGF-beta plus IL-4 increased IL-9 expression and downregulated Blimp-1

223 t cause NKT2 cells to constitutively produce IL-4 remain poorly defined.

224 signals might instruct NKT2 cells to produce IL-4.

225 e into TuAstrocytes, which, in turn, produce IL-4 that stimulates microglia to produce IGF1 to promot

226 The impact of the recombinantly produced IL-4 and IL-13 antagonist IL-4 mutein (IL-4M) on allergi

227 ingly, the miR-511-3p(low) DCs also promoted IL-4 secretion and suppressed IL-17 in cocultures with a

228 These provided IL-4, which targeted MCs to expand in the intestine.

229 eripheral blood neutrophils with recombinant IL-4 under conditions of hypoxia, and in vivo through th

230 Measurements and Main Results: IL-4 was elevated in human BAL from patients with acute

231 systemically administered serum albumin (SA)-IL-4 fusion protein leads to higher efficacy in preventi

232 In mice with chronic EAE, SA-IL-4 inhibits immune-cell infiltration into the spinal c

233 The SA-IL-4 fusion protein may be prophylactically and therapeu

234 We also show that the SA-IL-4 fusion protein prevents immune-cell infiltration in

235 nd T(H)2A-cell subsets, capable of secreting IL-4 and IL-21.

236 with low T cell mediated Leishmania-specific IL-4 and IL-10 responses, and consequently with high pro

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

238 nscription-factor signaling while supporting IL-4-STAT6-activated arginase 1 expression by promoting

239 0.001) in human keratinocytes and suppressed IL-4 and IL-13 by 68%-83% (P < 0.05) in mast cells.

240 Th9(IL-4+ IL-1beta) cells are phenotypically distinct T cell

241 t T cells compared to classic Th9 cells (Th9(IL-4+TGF-beta)) and other Th cells, and are enriched for

242 d with classic Th9(IL-4+TGF-beta) cells, Th9(IL-4+IL-1beta) cells are less exhausted, exhibit cytotox

243 Furthermore, when compared with classic Th9(IL-4+TGF-beta) cells, Th9(IL-4+IL-1beta) cells are less

244 ore striking anti-inflammatory function than IL-4-like cytokines and is essential for gill homeostasi

245 We further demonstrate that IL-4 limits neutrophil migration to inflamed joints, and

246 We demonstrate that IL-4/13A and IL-4/13B are required for the maintenance o

247 In this study, we find that IL-4 activation of different lineages of peritoneal macr

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

249 In addition, we found that IL-4 and IL-13 and Staphylococcus aureus lipoteichoic ac

250 We found that IL-4 and IL-13 engage a developmentally expressed IL-4Ra

251 Finally, we found that IL-4 is secreted by TuAstrocytes.

252 presence of various cytokines, we found that IL-4 significantly increases the surface expression of I

253 This study hypothesized that IL-4 regulates MMC9 development and MMC9-dependent exper

254 Our results show that IL-4 signaling is required for key pathogenic features o

255 RNA-seq analysis showed that IL-4 induced the expression of a program of genes includ

256 We demonstrated this concept by showing that IL-4 receptor signaling in mouse and human neutrophils i

257 ically activated macrophages (CAM s) and the IL-4-derived alternatively activated macrophages (AAM s)

258 le changes in lung; however, it elevated the IL-4 level and altered metabolites associated with fatty

259 tterns of major downstream regulators in the IL-4 signaling pathway.

260 RI]), the stem cell factor receptor KIT, the IL-4 system, and both Ca(2+)- and phosphatase-dependent

261 downregulation of the IFNgamma, but not the IL-4, gene.

262 PP-NKT cells produce the majority of the IL-4 in Peyer's patches and provide indirect help for B-

263 the low neutrophil surface expression of the IL-4 receptor alpha-chain (IL-4Ralpha), essential for IL

264 ticosteroids suggests that activation of the IL-4-HIF-1alpha-IL-13 axis might play a role in the deve

265 oglia, particularly mediating effects of the IL-4-regulated anti-inflammatory pathway, has important

266 ed IgG4 monoclonal antibody that targets the IL-4 receptor alpha chain (IL-4Ralpha), common to both I

267 these data together, we demonstrate that the IL-4 and CSF3 pathways are linked and play important rol

268 and molecular events that contributed to the IL-4-dependent decrease in parasitemia.

269 strains indicate that accessibility of these IL-4-induced regions can be regulated through difference

270 L-4 receptors, and their stimulation through IL-4 or IL-13 diminished their ability to form NETs and

271 ound that the hyporesponsiveness of AlvMs to IL-4 depended upon the lung environment but was independ

272 ients, transcripts of neutrophils exposed to IL-4/IL-13 and monocyte responses to IFN-gamma or IFN-be

273 ponsible for signaling following exposure to IL-4 and IL-13.

274 Urothelial exposure to IL-4 in vitro led to cell cycle polarization and increas

275 ncer, but associated mechanisms and links to IL-4 are largely unknown.

276 cells readily expressed Arg1 in response to IL-4 and/or IL-13, whereas skin or dLN fibroblasts faile

277 basis of chromatin remodeling in response to IL-4 stimulation in tissue-resident and monocyte-derived

278 glia, which showed an attenuated response to IL-4 when Trem2 expression was decreased.

279 determine conserved functional responses to IL-4 and IL-10.

280 both ICH models and were less responsive to IL-4 treatment.

281 the lungs, AlvMs regained responsiveness to IL-4 in a glycolysis-dependent manner.

282 lopment than the administration of wild-type IL-4 or of the clinically approved drug fingolimod.

283 e structures in mouse macrophages undergoing IL-4-mediated fusion.

284 f IL-13 pathways, but with near undetectable IL-4 expression.

285 ith CF and polarized to an M2 state by using IL-4, IL-10, glucocorticoids, apoptotic PMNs, or azithro

286 a novel, to our knowledge, function by which IL-4 and IL-13 cytokines condition thymic microenvironme

287 driving inflammation in the periphery, while IL-4 may merely have a central effect.

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

289 inflamed joints, and that CSF3 combined with IL-4 or IL-13 results in a prominent neutrophil up-regul

290 Treatment of human neutrophils with IL-4 suppressed HIF-1alpha-dependent hypoxic survival an

291 bone marrow-derived macrophages (BMM s) with IL-4 or TSG6 also induced M transition and expression of

292 ytokine IL-17A combined synergistically with IL-4 to increase DUOX2 expression in both colon and panc

293 IL-13 together with IL-4 failed to demonstrate any synergistic effect.

294 ostimulation with BCR agonists together with IL-4, whereas stimulated Duox1(-/-) cells showed attenua

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

296 imera models and wild-type mice treated with IL-4.

297 e; in contrast, inflamed lung treatment with IL-4 accelerated resolution through increased neutrophil

298 ty was sometimes increased by treatment with IL-4 or a beta-adrenergic receptor antagonist.

299 pathway is created by B cell treatment with IL-4 prior to BCR triggering.

300 eloped beyond stage 0 precursors and yielded IL-4-producing NKT2 cell subset but not IFN-gamma-produc