ライフサイエンスコーパス: IL-5

1 IL-5 and IL-13 are prominently secreted by group 2 innat

2 IL-5 and IL-13 showed strong correlations with AHR and m

3 IL-5 blockade or eosinophil depletion ameliorated coliti

4 IL-5 causes suspended eosinophils to polarize with filam

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

6 IL-5 enhances eosinophil adhesion and migration on perio

7 IL-5 increased proliferation, migration and colony tube

8 IL-5 is a major therapeutic target to reduce eosinophili

9 IL-5 neutralization before allergen challenge abolished

10 IL-5(+) pathogenic effector T(H)2 (peT(H)2) cells are a

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

12 of GMs = 0.25, 95% CI 0.10-0.62, P = 0.003; IL-5 GM = 0.55, 95% CI 0.30-0.99, P = 0.05; and IL-6 GM

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

14 osphorylated on Y705 (pSTAT3), IL-17, IL-13, IL-5, and IL-4 levels were measured in lung protein extr

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

16 Cytokine expression (IL-13, IL-5, IFN-gamma, and IL10) was measured in the supernata

17 IL-4, IL-13, IL-5, IFN-gamma, and TNF-alpha levels were measured in c

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

21 ies of polyfunctional Th2-like (CD4(+)IL-4(+)IL-5(+) and CD4(+)IL-2(+)IL-4(+)IL-5(+)TNF-alpha(+)) cel

22 CD4(+)IL-4(+)IL-5(+) and CD4(+)IL-2(+)IL-4(+)IL-5(+)TNF-alpha(+)) cells.

23 such as production of interleukin-4 (IL-4), IL-5, and IL-13 by whole-lung cells, in response to Pneu

24 g cytokines, including interleukin-4 (IL-4), IL-5, IL-9, IL-13, IL-31, and thymic stromal lymphopoiet

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

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

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

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

29 ulate the expression of TH2 cytokines, IL-4, IL-5 and IL-13.

30 ric mean (GM) levels of Th2 cytokines (IL-4, IL-5 and IL-6) for adults sensitized to Cladosporium wer

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

32 nocyte proliferation and production of IL-4, IL-5, and IFN-gamma in response to OVA and polyclonal ac

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

34 increase in CD4(+)IL-13(+) T cells and IL-4, IL-5, and IL-13 cytokines.

35 rgeting the canonical type 2 cytokines IL-4, IL-5, and IL-13 have shown consistent efficacy, especial

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

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

38 tly decreased levels of TH2 cytokines (IL-4, IL-5, and IL-13) but increased IFN-gamma levels in cell

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

42 2s, TC2 cells, and TH2 cells producing IL-4, IL-5, and IL-13, which induce mast cell, basophil, and e

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

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

45 activity in the skin and production of IL-4, IL-5, IL-10, and IL-13 are suppressed.

46 ) increases in parasite Ag-driven Th2 (IL-4, IL-5, IL-13), Th9 (IL-9), and the regulatory (IL-10) cyt

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

48 uction of IFN-gamma, TNF-alpha, IL-17, IL-4, IL-5, IL-13, and IL-10 was measured in the supernatants.

49 in the whole lung by increased pSTAT3, IL-4, IL-5, IL-13, and IL-17, and % CD4(+) T cells that produc

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

51 uction of several cytokines, including IL-4, IL-5, IL-13, eotaxin, IL-2, and IL-12 and the chemokines

52 frequency of CD4(+) T cells producing IL-4, IL-5, IL-2, and TNF-alpha in Fil(+)A(+) when compared wi

53 and TNF-RII), interleukin (IL)-1beta, IL-4, IL-5, IL-6, IL-10, and interferon gamma (IFN-gamma).

54 Serum cytokines (IL-4, IL-5, IL-6, IL-8, IL-10, TNF-alpha) were measured in 115

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

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

57 decreased levels of anti-inflammatory (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and TGF-beta) cy

58 levels of anti-inflammatory cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-27, IL-37, and transforming

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

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

61 B cells; CD23(+) (FcepsilonRII) cells; IL-4; IL-5; eosinophils, and vascular cell adhesion molecule 1

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

63 s in mice with eotaxin and/or interleukin 5 (IL-5) deficiency showed that FI-RSV vaccination did not

64 nts of inflammatory cytokines interleukin-5 (IL-5) and IL-13 in lung lavage fluid, decreased regulato

65 new class of drugs targeting Interleukin-5 (IL-5), an eosinophil growth, activation, and survival fa

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

67 of tumor necrosis factor-alpha, CXCL1, IL-6, IL-5, chemokine ligand 2, and IL-1beta.

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

69 apies, including blocking antibodies against IL-5, IL-13, IL-33, and thymic stromal lymphopoietin, as

70 ive capacity but down-regulated pro-allergic IL-5 secretion.

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

72 cytokines such as interleukin 10 (IL-10) and IL-5 and late-stage increases in Th1 cytokines such as I

73 'IL-13 and IL-5 high responders' class was strongly associated with

74 'IL-13 and IL-5 high responders' were at much higher risk of HDM se

75 92 cluster member miR-19a promoted IL-13 and IL-5 production and inhibited expression of several targ

76 0, signaling inhibitors that limit IL-13 and IL-5 production.

77 vel, cytokine patterns (especially IL-13 and IL-5), and clinical outcomes.

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

79 Low levels of TNF, TNF-RI, IL-1beta, and IL-5 and high levels of TNF-RII were associated statisti

80 dulating IL-10, CCL-17, CXCL9, IL-1beta, and IL-5 cytokines.

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

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

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

84 nd supported high IFN-gamma and low IL-4 and IL-5 production by T cells in Ag-specific stimulation as

85 , resulted in enhanced OVA-specific IL-4 and IL-5 secretion from DO11.10 CD4 TCs.

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

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

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

89 he levels of Th2 cytokines, such as IL-4 and IL-5.

90 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

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

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

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

94 o FcepsilonRIalpha were detected in 53%, and IL-5 or IL-13 responses in a minority of subjects with C

95 shortening, histology, and elevated IL-6 and IL-5 in colon tissues.

96 that LZTFL1 modulates T cell activation and IL-5 levels.

97 titers; MF59(R) induced strong antibody and IL-5 responses; GLA-SE induced antibodies and Th1; CAF01

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

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

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

101 F-alpha plus IFN-gamma, or IL-3, GM-CSF, and IL-5 alone significantly diminished the proapoptotic res

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

103 mmatory cell infiltration, eosinophilia, and IL-5 and IL-13 expression in the lung in a STAT6-indepen

104 n elicited the appearance of eosinophils and IL-5 in the airways of BALB/c but not C57BL/6 mice.

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

106 and intracellular markers (IL-10, Foxp3, and IL-5).

107 in eosinophils, goblet cell hyperplasia, and IL-5 levels.

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

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

110 with heightened type 2 immune responses and IL-5 and IL-13 production at the site of inflammation.

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

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

113 s from naive mice, which was blocked by anti-IL-5 antibody.

114 Humanized anti-IL-5 antibodies are effective in treating asthma patient

115 New anti-IL-5 therapeutics, mepolizumab and reslizumab, were US F

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

117 The effect of anti-IL-5 treatment on mature eosinophils and EoP numbers was

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

119 maternal or fetal administration of the anti-IL-5 neutralizing Ab, or a depleting Ab against ILCs, ca

120 eported that steady-state pulmonary rEos are IL-5-independent parenchymal Siglec-FintCD62L+CD101lo ce

121 ry eosinophils (iEos), which were defined as IL-5-dependent peribronchial Siglec-FhiCD62L-CD101hi cel

122 the eosinophil-activating cytokines, such as IL-5, IL-3, and GM-CSF, are typically present in atopic

123 N-gamma, TNF-alpha and IL-17alpha as well as IL-5, demonstrating that IL-33 has pleiotropic effects.

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

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

126 increased under this treatment, and blocking IL-5 with a neutralizing Ab ablated the IL-33-induced Eo

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

128 esponses and eNOS phosphorylation induced by IL-5.

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

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

131 he in the BM; instead, they are supported by IL-5.

132 h reduced expression of CCL24, CCL11, CCL20, IL-5, IL-13, IL-25, TGFB, and TSLP.

133 d the highest levels of innate immune cells, IL-5, type 17-related immune mediators, and activated T

134 related inversely with PNIF after challenge (IL-5, r = -0.79, P < 0.0001; IL-13, r = -0.60, P = 0.006

135 ess colitic inflammation and reduced colonic IL-5 and eosinophil numbers to levels seen in wild-type

136 Cytokine (IL-5) levels in BAL fluid also increased markedly follow

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

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

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

140 production of the T helper type 2 cytokines IL-5 and IL-13.

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

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

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

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

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

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

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

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

149 In the SCIT group, decreased IL-5 production was observed starting 10 months after tr

150 5-deficient mice, we found that ILC2-derived IL-5 is critically involved in the enhanced production o

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

152 eron-gamma (IFN-gamma) and the loci encoding IL-5 and IL-13.

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

154 d responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production.

155 mice were treated with a plasmid expressing IL-5 (pIL5) or an empty plasmid control via hydrodynamic

156 Nasal fluid IL-5 and IL-13 correlated inversely with PNIF after chal

157 dentified via expression profiling following IL-5 stimulation.

158 = 0.5165 for IL-4; p < 0.001, r = 0.5544 for IL-5; and p < 0.001, r = 0.4901 for IL-13) and levels of

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

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

161 y using blocking Abs and ILC2s isolated from IL-5-deficient mice, we found that ILC2-derived IL-5 is

162 (e.g. sCD23 down by 50%)/TH2 cytokines (e.g. IL-5 down by 70%)/ADAM8-positive eosinophils (down by 60

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

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

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

166 eT(H)2 cells expressed significantly greater IL-5 and IL-13 than did hematopoietic prostaglandin D sy

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

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

169 PBMCs from allergic subjects exhibit higher IL-5 and IL-10 responses in season than when collected o

170 (H) polarizing cytokines IL-12p70, IFNgamma, IL-5, IL-13, IL-23, and IL-6 production in vivo.

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

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

173 anges on a cellular level were a decrease in IL-5 in the SCIT group and a significant, transient incr

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

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

176 The homeostatic hypereosinophilia seen in IL-5-transgenic mice was significantly lower with ST2 de

177 Group 2 innate lymphoid cells (ILC2) include IL-5- and IL-13-producing CRTh2(+)CD127(+)cells that are

178 ammatory cytokines and chemokines, including IL-5, thymic stromal lymphopoietin and CCL11, that help

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

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

181 reover, lung inflammation leads to increased IL-5 production by type 2 cytokine-producing innate lymp

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

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

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

185 first to report a role for helminth-induced IL-5 and IL-33 in protection against autoimmunity.

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

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

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

189 Finally, a PGI2 analog inhibited IL-5 and IL-13 expression by human ILC2s that were stimu

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

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

192 We demonstrate that PGI2 inhibits IL-5 and IL-13 protein expression by IL-33-stimulated IL

193 nd food allergen produced significantly less IL-5, greater IL-10 levels, and increased numbers of reg

194 rgic subjects, as expected we observed lower IL-5 responses and robust production of IFN-gamma compar

195 f subtilisin into the airways increased lung IL-5-producing type 2 innate lymphoid cells, which requi

196 og inhibited Alternaria extract-induced lung IL-5 and IL-13 protein expression, and reduced the numbe

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

198 n expression, and reduced the number of lung IL-5- and IL-13-expressing ILC2s and the mean fluorescen

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

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

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

202 ncluding nuclear structure, surface markers, IL-5 independence, and immunoregulatory function that is

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

204 ls with humanized antibodies that neutralize IL-5, a potent eosinophil growth, activation, and surviv

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

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

207 ent of bone marrow cells with IL-33, but not IL-5, led to specific early expansion of IL-5Ralpha-expr

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

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

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

211 nnate lymphoid cells produce high amounts of IL-5 and IL-13, thereby contributing to type 2-mediated

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

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

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

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

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

217 nd is associated with cutaneous expansion of IL-5-producing type 2 innate lymphoid cells.

218 2s) in the lungs showed robust expression of IL-5 after Alternaria exposure.

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

220 Expression of IL-5 and IL-33 increased rapidly in the lungs, but not i

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

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

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

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

225 ILC2s and the mean fluorescence intensity of IL-5 and IL-13 staining.

226 ere unable to increase their serum levels of IL-5 and allergen-induced eosinophilopoiesis in the bone

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

228 lls from FHL2-KO mice show reduced levels of IL-5 and IL-13.

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

230 educed the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enh

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

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

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

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

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

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

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

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

239 at IL-33 induced the increased production of IL-5 and IL-13 from splenocytes and liver mononuclear ce

240 activation of ILC2s and their production of IL-5, plays a key role in promoting acute reactive eosin

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

242 No significant reduction of IL-5 was observed in the SLIT or untreated group.

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

244 Given the role of IL-5 produced by ILC2 in regulating eosinophil developme

245 ts after in vitro expansion for secretion of IL-5 (a representative Th2 cytokine) and IFN-gamma (Th1)

246 a cell-intrinsic defect in the secretion of IL-5 and IL-13 in response to innate stimuli, resulting

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

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

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

250 ated autoimmunity, and this was dependent on IL-5.

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

252 In this study, we show that only IL-5 induces differentiation of eosinophils from bone ma

253 IFN-gamma or IL-12 if activated by IL-2, or IL-5 if activated by IL-4.

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

255 igh titers from the lungs of eotaxin- and/or IL-5-deficient mice.

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

257 We establish that, unlike GM-CSF or IL-5, IL-3 triggers prolonged signaling through activati

258 ion in cells activated with IL-3, GM-CSF, or IL-5.

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

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

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

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

263 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although

264 nate lymphoid cells (ILC2s) robustly produce IL-5 and IL-13, cytokines central to the asthma phenotyp

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

266 and IL-17, and % CD4(+) T cells that produce IL-5, IL-13, and IL-17.

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

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

269 Whereas R848 significantly reduced IL-5, IL-13, and IL-17, it induced IFN-gamma and IL-27.

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

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

272 rect target of IL-33, which instead requires IL-5 for activation.

273 Serum IL-5 and IL-13 are reliable biomarkers for the blood eos

274 Serum IL-5 and IL-13 were the two best, followed by EDN as sep

275 At 24 months, T cell responses showed IL-5 levels significantly below the before-treatment bas

276 t patients with NA, significantly suppressed IL-5, IL-13, and IFN-gamma secretion.

277 Systemic IL-5 was also increased under this treatment, and blocki

278 IL-33 supports EoMs by driving both systemic IL-5 production and the expansion of IL-5Ralpha-expressi

279 iency despite similar elevations in systemic IL-5.

280 Targeting IL-5-driven eosinophil differentiation locally within th

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

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

283 We also discovered that IL-5, a cytokine produced by activated immune cells, act

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

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

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

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

288 sthmatics demonstrated a greater response to IL-5 than mild asthmatics.

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

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

291 Whereas IL-5 is crucial for supporting mature eosinophils (EoMs)

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

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

294 nophils from bone marrow precursors, whereas IL-5, GM-CSF, and to a lesser extent IL-3 promote surviv

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

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

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

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

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

300 d significantly with IFN-gamma, but not with IL-5, IL-13, IL-17, or TNF-alpha.