ライフサイエンスコーパス: IL-5

1 IL-5 and IL-13 markedly increased eosinophil numbers loc

2 IL-5 causes suspended eosinophils to polarize with filam

3 IL-5 circumsporozoite protein (CSP) ratios, a helper T c

4 IL-5 enhances eosinophil adhesion and migration on perio

5 IL-5 increased proliferation, migration and colony tube

6 IL-5 increased the number of eosinophils in BM and lung

7 IL-5 neutralization before allergen challenge abolished

8 IL-5 stimulation of plasma cells in vitro induced change

9 IL-5-induced angiogenic responses depended on the bindin

10 erleukin (IL) levels of IL-12, IL-17, IL-10, IL-5, CXCL9, E-Selectin and ST2/IL-1R4; and decreased le

11 (TNF-alpha), IL-6, IL-12/23, IL-17, IL-4/13, IL-5, immunoglobulin E (IgE), integrins and B cells.

12 olar lavage lymphocytes, eosinophils, IL-13, IL-5, and eotaxin were reduced in ROCK2(+/-) vs. wild-ty

13 s of OVA on lymphocytes, eosinophils, IL-13, IL-5, and mucous hypersecretion to wild-type levels, whe

14 day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased numbers of

15 n inflammatory factors (TNF-alpha, IL-1beta, IL-5) and suppressive immune populations (myeloid-derive

16 e modulating protumoral IL-1alpha, IL-1beta, IL-5, IL-6 and IL-17 and antitumoral IL-2 and IL-12 in t

17 ammatory cytokines and chemokines (IL-1beta, IL-5, IL-6, TNF-alpha, RANTES, MIP-1beta, MCP-1, KC and

18 a TH2-dominated microenvironment (eotaxin-2, IL-5, IL-18, and IL-13) and increased signalling molecul

19 GATA-3, IL-5 and eotaxin mRNA expression decreased significantly

20 spectrometry following treatment with IL-3, IL-5 or granulocyte-macrophage colony-stimulating factor

21 of apoptosis could be due to released IL-3, IL-5, and GM-CSF found in supernatants.

22 5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

23 eanut-specific highly differentiated IL-4(+) IL-5(+) Th2 cells.

24 ne activity, including interleukin-4 (IL-4), IL-5, and IL-13, are now established biological mechanis

25 with type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13, which promote airway eosinophilia, mucu

26 of the type 2 cytokines interleukin (IL)-4, IL-5 and IL-13 from T helper 2 (Th2) cells and innate ly

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

28 by the type 2 cytokines Interleukin-(IL)-4, IL-5, and IL-13.

29 The type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 have important roles in stimulating

30 MNs-CIT regulated Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory cytokines (IL-10) in

31 by the release of signature cytokines IL-4, IL-5 and IL-13 from cells of both the innate and adaptiv

32 f ILC2s restored eosinophil influx and IL-4, IL-5 and IL-13 production in lung tissue, as well as TH2

33 -12, interferon-gamma) and T-helper 2 (IL-4, IL-5) cytokines by 2 years of age were measured in child

34 ficient mice secreted higher levels of IL-4, IL-5, and GM-CSF.

35 chemokine/CCL17), and the synthesis of IL-4, IL-5, and IL-13 by T cells, in the course of the mixed l

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

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

38 d levels of proinflammatory cytokines (IL-4, IL-5, and IL-13) and decreased goblet cell hyperplasia.

39 naling among classical TH 2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1)

40 ammation is mediated by TH2 cytokines (IL-4, IL-5, and IL-13).

41 r, eosinophilia, protein level of lung IL-4, IL-5, and IL-13, and airway mucus score were also signif

42 sease through release of the cytokines IL-4, IL-5, and IL-13, resulting in increased airway eosinophi

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

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

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

46 n by the prototypical type 2 cytokines IL-4, IL-5, and IL-13.

47 examined gamma interferon (IFN-gamma), IL-4, IL-5, and IL-17 production by lung lymphocytes in immuno

48 mice, TGFbeta1-mim downregulated IL-2, IL-4, IL-5, IL-13, and IFN-gamma, upregulated IL-10, and induc

49 e eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE production.

50 tokines (thymic stromal lymphopoietin, IL-4, IL-5, IL-13, and the itch-specific cytokine IL-31 and th

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

52 reporting on levels of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamm

53 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, CCL2,

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

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

56 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from patients

57 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from patients

58 on (eosinophilia, eotaxin-2 expression, IL-4/IL-5/IL-13 production, mucus production) in the airways

59 a signaling and defined that IL-4Ralpha(-/-)/IL-5(-/-) double-knockout mice displayed significant eos

60 ls) are the primary source of interleukin 5 (IL-5) and IL-13 during type 2 (allergic) inflammation in

61 elper type-2 (Th2) [increased interleukin 5 (IL-5) and interleukin 13 (IL-13)] and T regulatory type-

62 ntiation assay, we found that interleukin 5 (IL-5) supports the generation of Ly6G(+) eosinophils fro

63 oped a 5-plex assay measuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), int

64 Interleukin-5 (IL-5) is the key cytokine for eosinophils and we have pr

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

66 are accompanied by a dramatic interleukin-5 (IL-5)-dependent increase in eosinophilia and evidence of

67 -inflammatory cytokine (TNF, IL-1beta, IL-6, IL-5 and CXCL1) levels were significantly lower in LysMc

68 dy-associated cytokines (interleukin [IL] 6, IL-5, and IL-10), nAb titers were higher in epidemic KS

69 -13, the resolution of inflammation by IL-9, IL-5-induced eosinophil expansion, IL-33-mediated macrop

70 In addition, IL-5-induced neo-vascular formation was verified in both

71 Yearly vaccination against IL-5 may be a long-term solution for the treatment of IB

72 RATIONALE: Mepolizumab, an IL-5-blocking antibody, reduces exacerbations in patient

73 ncreased proportions of ILC2s (P = .002) and IL-5(+) cells (P = .042), IL-13(+) cells (P = .042), and

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

75 rkers including ATP, ACh, nitrite, MCP-1 and IL-5 and participants' confounders, age and gender, in p

76 ted with an enhanced expression of IL-10 and IL-5.

77 92 cluster member miR-19a promoted IL-13 and IL-5 production and inhibited expression of several targ

78 0, signaling inhibitors that limit IL-13 and IL-5 production.

79 A higher secretion of IL-13 and IL-5 was detected in presence of the culprit drug compar

80 -CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) subject-to-subject variation.

81 Interleukin (IL) 2 and IL-5 ratios were associated with RTS,S/AS01E vaccination

82 the resolution of inflammation, and IL-3 and IL-5 may also have such properties.

83 GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 55

84 eta common chain cytokines GM-CSF, IL-3, and IL-5 regulate varied inflammatory responses that promote

85 transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and id

86 production of the type 2 cytokines IL-33 and IL-5, which promoted accumulation of eosinophils.

87 hils and their associated cytokines IL-4 and IL-5 are emerging as central orchestrators of the immune

88 t not TB antigen-stimulated type 2 (IL-4 and IL-5) and regulatory (transforming growth factor beta [T

89 amma) as compared to Th2 cytokines (IL-4 and IL-5) in splenocyte culture supernatants of the micronee

90 expression of TH2 cytokines (IL-13, IL-4 and IL-5).

91 vage fluid released lower levels of IL-4 and IL-5, and these results were paralleled by decreased pro

92 reased bronchoalveolar lavage fluid IL-4 and IL-5, whereas adoptive transfer of wild-type CD19(+)CD13

93 n expression of IL-1ra, P-Selectin, IL-4 and IL-5; ZIKV-infected donors demonstrated variation in exp

94 s well as the production of IL-13, IL-4, and IL-5 by T cells in the course of the MLR, was further en

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

96 while minimal changes were seen in IL-4- and IL-5-positive cells.

97 Serum levels of IL-5 and IL-5 receptor alpha, but not IgE, were similarly increas

98 A combination of urinary ATP and IL-5 plus age and gender was shown to have clinically ac

99 tween the Ig-superfamily receptor CD300f and IL-5 is a key checkpoint that modifies the ability of eo

100 ymphoid cells and IL-13(+)CD4(+) T cells and IL-5 and IL-13 production by lymph node cells but had no

101 head box P3-positive regulatory T cells, and IL-5(+) ILC2s.

102 M-CSF or IL-5 alone, loss of both GM-CSF and IL-5 signaling impaired protection against H. polygyrus

103 GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil g

104 a (CSF2RB) chain family cytokines GM-CSF and IL-5.

105 was observed between blood eosinophilia and IL-5, IL-13, and eosinophil-derived neurotoxin (EDN), wh

106 sociation between epithelial eosinophils and IL-5 concentrations in nasal secretion (r = 0.69, P = .0

107 Nasal tissue eosinophils and IL-5 in nasal secretion increased significantly after RA

108 ype mice markedly boosted ILC2 expansion and IL-5/IL-13 generation in a CysLT2R-dependent manner.

109 Unexpectedly, the mRNA for GATA3 and IL-5 correlated better with mRNA for CD30, TNFR2, ICOS,

110 nificantly increased the numbers of ILC2 and IL-5 and IL-13 expression by ILC2 in the lung.

111 Expansion of ILC2s and IL-5/IL-13 generation reflected CysLT2R-dependent produc

112 prost inhibited CD4 T cell proliferation and IL-5 and IL-13 expression in vitro, and IP deficiency di

113 enhanced allogeneic T cell proliferation and IL-5, IL-9, and IL-13 production compared with native Ab

114 s of thymic stromal lymphopoietin (TSLP) and IL-5 in the skin.

115 Anti-IL-5 therapy is a potential treatment for patients with

116 Anti-IL-5 treatment attenuated eosinophils and prevented the

117 ic therapies, anti-IgE (omalizumab) and anti-IL-5 antibodies (mepolizumab), are used in the treatment

118 tion to targeting eosinophils, IL-5 and anti-IL-5 biologics may have a direct role on AEC.

119 rease in sputum IL-5 has been detected, anti-IL-5 therapies are not effective in preventing exacerbat

120 acebo-controlled trial of the humanized anti-IL-5 antibody, reslizumab, (1.0 mg/kg IV) administered 3

121 Reslizumab is a humanized anti-IL-5 monoclonal antibody used as add-on maintenance trea

122 To determine the effect of anti-IL-5 antibody on the numbers and phenotypes of allergen-

123 P), systemic corticosteroids (Pred), or anti-IL-5.

124 ic asthma for more than a decade, three anti-IL-5 biologics and one anti-IL-4R biologic have recently

125 sinophilic asthma who do not respond to anti-IL-5 therapies.

126 were depleted in asthma patients using anti-IL-5 (mepolizumab), followed by a challenge with rhinovi

127 cent advances in asthma management with anti-IL-5 therapies, many patients have eosinophilic asthma t

128 he high-level production of IL-10 as well as IL-5 and small amounts of the related cytokines IL-4 and

129 expression in CD4 T cells in vivo attenuates IL-5 synthesis in the lung that is accompanied by dimini

130 Expression of PD-1, PD-L1, PD-L2, TGF-beta, IL-5, and IL-10 mRNA was measured by real-time quantitat

131 se findings highlight the cross-talk between IL-5 receptor and CD300f as a novel pathway regulating a

132 Both IL-5 neutralization and STAT5 inhibition blunted the eff

133 res a common beta subunit receptor with both IL-5 and GM-CSF but, through alpha-subunit-specific prop

134 show that the metabolic programme driven by IL-5 is dependent on the STAT5/PI3K/Akt signalling axis

135 esponses and eNOS phosphorylation induced by IL-5.

136 associated skin inflammation was mediated by IL-5-expressing pathogenic effector Th2 cells and was in

137 Dermal-epidermal separation by IL-5-activated eosinophils depends on adhesion and Fcgam

138 er IL-4R-dependent or IL-4R-independent/CCR3/IL-5-dependent immunity influenced B. malayi microfilari

139 , thymus and activation-regulated chemokine, IL-5, and thymic stromal lymphopoietin levels were signi

140 g release of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymphoid cells

141 tic ILC2s that produced the type 2 cytokines IL-5 and IL-13 during liver inflammation.

142 s well as production of the type 2 cytokines IL-5 and IL-13, from human tonsillar and blood ILC2s in

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

144 ation, and secretion of the type 2 cytokines IL-5, IL-9 and IL-13 that was dependent on cell-intrinsi

145 n of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13.

146 of the ILC2-driven proinflammatory cytokines IL-5 and IL-13 both in vitro and in vivo.

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

148 s found worldwide is driven by the cytokines IL-5 and IL-13 coming from Th2 cells, type 2 innate lymp

149 d eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to mu

150 ociated with elevations in type 2 cytokines (IL-5 and IL-13) and the type 1 cytokine, IFN-gamma.

151 eceptors, CD69, CD44, and CD23 and decreased IL-5 and eotaxin receptors than blood eosinophils.

152 Bcl-6 binding to the IL-5 gene and decreased IL-5 mRNA expression.

153 support enhanced TH1 responses and decreased IL-5 responses.

154 /-) , but not Esr2(-/-) , mice had decreased IL-5 and IL-13 production, BAL eosinophils, and IL-33 re

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

156 of Th2, Th9, Th17/Th22 polar cytokines (i.e. IL-5, IL-13, IL-9, IL-17, IL-22).

157 HSP70-1 overexpression enhanced IL-5-induced angiogenic responses.

158 e that in addition to targeting eosinophils, IL-5 and anti-IL-5 biologics may have a direct role on A

159 The vaccine consisted of equine IL-5 (eIL-5) covalently linked to a cucumber mosaic viru

160 decreased the number of lung ILC2 expressing IL-5 and IL-13 following Alt-Ext-challenge compared to W

161 dentified via expression profiling following IL-5 stimulation.

162 lues of 0.99, 0.93, 0.99, 0.96, and 0.75 for IL-5, IL-6, IL-10, IL-22, and TNFalpha, respectively.

163 Eosinophil receptors for IL-5 share a common ss-chain with IL-3 and GM-CSF recept

164 We report a pivotal role for IL-5 as an angiogenic activator.

165 face expression of IL-5Ralpha and functional IL-5 signaling.

166 production of gamma interferon (IFN-gamma), IL-5, IL-9, IL-17, and IL-22 and decreased production of

167 a substantial and rapid source of IFN-gamma, IL-5 and IL-13, and IL-17A or IL-22, respectively.

168 Notch-deprived mice produced less IFN-gamma, IL-5, and IL-13 than wild-type cells.

169 were associated with secretion of IFN-gamma, IL-5, and/or IL-4.

170 elated with lower frequencies of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expre

171 n unusual cytokine profile (IL-13(hi)IL-4(hi)IL-5(hi)IL-21(lo)) and coexpress the transcription facto

172 High IL-5 levels may reflect a Th2 environment associated wit

173 te Cox proportional hazards regression, high IL-5 (hazard ratio [HR], 5.76 [95% confidence interval {

174 Lung ILC2, IL-5 and IL-13 production, and BAL inflammatory cells we

175 C1 and increased numbers of immunopathologic IL-5(+) and IL-13(+) ILC2 and IL-17A(+) ILC3 compared wi

176 The angiogenic effects were confirmed in IL-5-deficient mice and addition of IL-5 antibody.

177 uished from CRSwNP by profound elevations in IL-5, IL-6, IL-13, and IFN-gamma; however, significant h

178 anscription factor AP-1 was a main factor in IL-5-induced HSP70-1 in response to ERK and AKT signalin

179 IFN-gamma-positive cells, and an increase in IL-5-positive cells, but did not impact clearance of Pne

180 lted in tissue eosinophilia and increases in IL-5 but no structural changes.

181 vealed that CD8gamma13 polarization included IL-5 in addition to IFN-gamma and IL-13.

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

183 s (ILC2) are stimulated by IL-33 to increase IL-5 and IL-13 production and airway inflammation.

184 evere atopy was associated with an increased IL-5/IFN-gamma ratio.

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

186 o CD11c-restricted Wnt4 deficiency increased IL-5 production, group 2 innate lymphoid cell expansion,

187 PD-L2 mAb blockade significantly increased IL-5(+) T cells in culture.

188 mation of EETs was associated with increased IL-5 (P < .05) and periostin (P < .05) tissue levels and

189 effect of indomethacin on STAT6-independent IL-5 and IL-13 responses in vivo.

190 ilarial infection and that IL-4R-independent/IL-5- and CCR3-dependent pathways are sufficient to cont

191 on of RA, which acts on T(H) cells to induce IL-5 and gut-homing integrin.

192 RTS,S/AS01E-induced IL-5 may be a surrogate of lack of protection, whereas T

193 TLR4, and TLR6, and TLR stimulation induced IL-5 and IL-13 production.

194 , group 2 innate lymphoid cell infiltration, IL-5 and IL-13 production, as well as IL-17A(+) CD4 T ce

195 LF) and tissue eosinophils and inflammation, IL-5, IL-13 and AHR.

196 IL-35 inhibited IL-5 and IL-13 production by ILC2s in the presence of IL

197 secretion of IFN-gamma whereas it inhibited IL-5 and IL-13, demonstrating its direct effect on atten

198 B-1 cell-intrinsic PD-L2 expression inhibits IL-5 production by T cells and thereby limits natural Ab

199 by introducing the dystrophin mutation into IL-5 transgenic mice.

200 PGI2 signaling significantly inhibited lung IL-5 and IL-13 protein expression, and reduced the numbe

201 n expression, and reduced the number of lung IL-5- and IL-13-expressing ILC2s, as well as the mean fl

202 eukin (IL)-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway h

203 ung inflammation, with an increase in mainly IL-5- and IL-13-producing but not IL-4-producing TH2 cel

204 Migrating IL-5-activated eosinophils on periostin exhibit loss of

205 mmation and airway dysfunction by modulating IL-5 expression via binding to and inhibiting the repres

206 manized monoclonal antibody that neutralizes IL-5 and efficiently attenuates eosinophils, proved clin

207 smooth muscle cells, IL-13 and IL-4, but not IL-5 and IL-17A, enhanced the histamine-induced Ca(2+) m

208 ted mice produced IFN-gamma and IL-2 but not IL-5 on stimulation with the aforementioned peptides.

209 IL-4, but not IL-5 or IL-17A, also increased the potency of histamine.

210 (two cytokines implicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33.

211 mphopoietin (TSLP), IL-9, and IL-13, but not IL-5, in bronchoalveolar lavage fluid.

212 Of note, IL-5 mRNA expression was significantly increased in puri

213 irmed in IL-5-deficient mice and addition of IL-5 antibody.

214 the blood and airway after administration of IL-5 neutralizing antibodies has not been reported.

215 Administration of IL-5, a major ILC2 product, was sufficient to repress ag

216 ient's PBMC produced a substantial amount of IL-5 and IL-13 in response to these flour extracts.

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

218 ase of specific and total IgE, as well as of IL-5 in serum.

219 Our data demonstrate that binding of IL-5 to IL-5Ralpha receptors enhances angiogenic respons

220 ronchoalveolar lavage fluid concentration of IL-5, a cytokine associated with eosinophil differentiat

221 i-Siglec antibody led to robust depletion of IL-5-induced eosinophilia in vivo.

222 Mechanistically, differentiation of IL-5-producing Zc3h12a(-/-) TH2 cells is mediated throug

223 nhanced by priming with physiologic doses of IL-5.

224 hilia in FE is secondary to dysregulation of IL-5 production in PBMC (and their component subsets).

225 This was not a direct effect of IL-5, as IL-5TgDeltadblGATA1 mice were protected from DC

226 Treatment did reduce gene expression of IL-5 and IL-10 by lung leukocytes and promoted sustained

227 as found between PD-1 mRNA and expression of IL-5 mRNA in control nasal tissue (r = 0.95, P < 0.0001)

228 P1 regulates the development and function of IL-5-producing TH2 cells through the Notch/Gata3 pathway

229 This exacerbation includes increase of IL-5, IL-13, eotaxin and MCP-3; infiltration of eosinoph

230 s well as the mean fluorescence intensity of IL-5 and IL-13 staining.

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

232 Prodigious levels of IL-5 and IL-13 were confined to HPGDS+ CRTH2+IL-17RB+FFA

233 Serum levels of IL-5 and IL-5 receptor alpha, but not IgE, were similarl

234 from HDM-allergics produced higher levels of IL-5 whereas non-HDM-sensitized individuals mounted high

235 ) B cells had significantly higher levels of IL-5, a potent stimulator of B-1 cell Ab production.

236 Additionally, levels of IL-5, but no other cytokine, increased with age and corr

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

238 ed morphology evolves to foster migration of IL-5-stimulated eosinophils on a surface coated with per

239 Anti-ADAM8 inhibited migration of IL-5-stimulated eosinophils on periostin.

240 n IL-33(-/-) mice and upon neutralization of IL-5.

241 ed killing of eosinophils in the presence of IL-5 might lead to increased efficacy in patients with I

242 After 10 minutes in the presence of IL-5, adherent eosinophils were polarized with PSGL-1 at

243 oid cells (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge t

244 s) were identified as the major producers of IL-5 and IL-13 in response to IL-25.

245 A-dependent 4-fold increase in production of IL-5 and expression of integrin alpha(4)beta(7).

246 a marked reduction in cytokine production of IL-5 and IL-13 while TGF-beta had no effect on ILC2 cyto

247 nd hyperresponsiveness through production of IL-5, IL-13 and VEGFA.

248 K1/2 MAPK pathways reduced the production of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response t

249 trophils, along with increased production of IL-5, prostaglandin D2, and eosinophil and T-helper type

250 To explore the role of IL-5 driven eosinophilia in post-DEC reactions, 8 adults

251 We sought to determine the role of IL-5 priming and identify the signaling molecules involv

252 ILC2 represent a major innate cell source of IL-5 and IL-13 required for mounting atheroprotective im

253 Eosinophils from the spleens of IL-5 transgenic mice, fluorescently labeled ex vivo, wer

254 Finally, engagement of Siglec-8 on IL-5-primed eosinophils resulted in increased phosphoryl

255 that NEI had a higher stimulatory effect on IL-5, IL-10, IL-17 responses.

256 ctions uniquely as an activating receptor on IL-5-primed eosinophils through a novel pathway involvin

257 te regulatory mechanism, which is reliant on IL-5-induced lung eosinophilia, ultimately limiting the

258 and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h.

259 Therapeutic targeting of IL-33 or IL-5 reversed NK cell suppression and alleviated cancer

260 Treatment with antibodies targeting IL-5 or IL-5 receptor alpha reduces the frequency of asthma exac

261 animals were highly dependent on Th cells or IL-5.

262 In contrast to deficiency in GM-CSF or IL-5 alone, loss of both GM-CSF and IL-5 signaling impai

263 ls after in vitro stimulation with GM-CSF or IL-5.

264 eosinophils from NDs and EOs after overnight IL-5 priming.

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

266 Plasma IL-5 (P = .0008) and IL-10 (P = .0089) were lower in tho

267 High plasma IL-5 and IL-7 levels pre-ART were associated with increa

268 Further, CysLTs directly potentiated IL-5 and IL-13 production from purified ILC2s stimulated

269 (RORC) 2, and RORalpha; were able to produce IL-5, IL-13, and IL-4; and, accordingly, were characteri

270 ng expressed the IL-25 receptor and produced IL-5 and IL-13.

271 h increased interleukin-4 (IL-4) production, IL-5 transcription, and eosinophilia.

272 ed KLRG1(+) ILC2s proliferation but promoted IL-5 expression.

273 H)1/IFN-gamma, OASL, and T(H)2/IL-4 receptor/IL-5 skewing, although less than seen in patients with A

274 PIP1; encoded by the Zc3h12a gene) regulates IL-5-producing TH2 cell differentiation and TH2-mediated

275 ciencies to determine which of the remaining IL-5- or IL-17A-producing lymphocyte subsets dominated t

276 Serum IL-5 and IL-13 decreased during climate treatment in ast

277 uncertain as, although an increase in sputum IL-5 has been detected, anti-IL-5 therapies are not effe

278 with IL-33 and neuromedin U (NMU) supported IL-5 but constrained IL-13 expression and ILC2 prolifera

279 Treatment with antibodies targeting IL-5 or IL-5 receptor alpha reduces the frequency of ast

280 and we have previously shown that targeting IL-5 by vaccination reduces disease symptoms in horses.

281 We tested IL-5-primed mouse bone marrow-derived and human blood-so

282 ently reported that IL-3 is more potent than IL-5 or GM-CSF in maintaining the ERK/p90S6K/RPS6 riboso

283 Our results provide evidence that IL-5-activated eosinophils directly contribute to BP bli

284 We found that IL-5 and IL-13 were expressed not only by CRTH2(+) but a

285 We found that HBEC expressed the IL-5 receptor, which triggered intracellular signaling a

286 s resulted in increased Bcl-6 binding to the IL-5 gene and decreased IL-5 mRNA expression.

287 with IL-5Ralpha function determined through IL-5 stimulation and subsequent RNA sequencing and quant

288 associated with disease severity and tissue IL-5 expression but unrelated to the patients' atopy sta

289 When compared to IL-5, continuing exposure to IL-3 further induced degran

290 cted from subsequent malaria, in contrast to IL-5 and RANTES, which increased the odds of malaria.

291 In addition, unlike IL-5 or GM-CSF, IL-3 induced expression of CD32B/C (FCGR

292 cells from affected family members, as were IL-5 protein levels in supernatants from both stimulated

293 Whereas IL-5 mRNA expression was significantly increased in fres

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

295 GATA1 mice were protected from DCMi, whereas IL-5(-/-) mice exhibited DCMi comparable with WT mice.

296 This observation may explain why IL-5 neutralization reduces but does not completely erad

297 nts compared to controls (all P < .05), with IL-5 and IL-7 significant after Bonferroni-Holm correcti

298 Following activation with IL-5 and in the presence of BP autoantibodies, eosinophi

299 of EBI2 ligands alone or in combination with IL-5 priming to induce the migration of human blood Eos

300 lead to increased efficacy in patients with IL-5-driven eosinophilia.

301 ast, killing of purified eosinophils without IL-5 was only seen in EOs, and natural killer cell-media