ライフサイエンスコーパス: anti-IgE

1 nd monocytes were stimulated up to 21 h with anti-IgE.

2 bidity, and, for those with allergic asthma, anti-IgE.

3 t cells after low-intensity stimulation with anti-IgE.

4 A) quantified IgG anti-Fc epsilonRIalpha and anti-IgE.

5 hibited histamine release elicited by PMA or anti-IgE.

6 treatments: cromones, antileukotrienes, and anti-IgE.

7 g responses to intradermal administration of anti-IgE.

8 th long-acting beta-adrenergic agonists, and anti-IgE.

9 or histamine in cultures activated with IL-3/anti-IgE.

10 unoreactive MIP-1alpha upon stimulation with anti-IgE.

11 nes significantly upregulated after repeated anti-IgE.

12 ved mast cells were treated for 2 weeks with anti-IgE.

13 scribed basophil-activating stimuli IL-3 and anti-IgE.

14 in association with ICS, 53.3% LTRAs, 64.1% anti-IgE, 10.7% theophylline, and 16.0% oral corticoster

15 ve sensitization with IgE and challenge with anti-IgE; 2) preincubation with IL-4 enhanced IgE-depend

16 as removed from intestinal wash samples with anti-IgE (A2)-Sepharose.

17 -dependent fashion following activation with anti-IgE Ab (10 ng/ml).

18 lood-derived mast cells were stimulated with anti-IgE Ab in the presence of dexamethasone or FK506.

19 dermal challenge with high concentrations of anti-IgE Ab induced an ear-swelling response in these st

20 FcgammaRIII pathway involving recognition of anti-IgE Ab itself.

21 in vitro release of this cytokine induced by anti-IgE Ab or by the human recombinant histamine-releas

22 s, did not secrete IL-4 when stimulated with anti-IgE Ab or soluble parasite Ag.

23 Stimulation with anti-IgE Ab resulted in the phosphorylation of ERKs, whi

24 the cells to IgE-mediated stimulation using anti-IgE Ab was marginally decreased (approximately 40%)

25 during an escalating series of stimulation (anti-IgE Ab) and that expression loss occurred despite t

26 ulation of human basophils with a polyclonal anti-IgE Ab, early signaling elements showed sustained p

27 e in strict proportion to release induced by anti-IgE Ab.

28 ith the more profound loss of Syk induced by anti-IgE Ab.

29 in cultures activated with 1 or 100 ng/ml of anti-IgE Ab.

30 g in cultures stimulated for 16 to 20 h with anti-IgE Ab.

31 Treatment of allergic patients with anti-IgE Abs has been shown to induce a decrease in Fcep

32 argeting surface-bound IgE with low-affinity anti-IgE Abs is capable of suppressing allergic reactivi

33 c disease by decreasing circulating IgE with anti-IgE Abs is currently under clinical study.

34 utrophils also released MMP-9 in response to anti-IgE Abs, and agonist Abs against FcepsilonRI, Fceps

35 from cells triggered with IgE-specific Ag or anti-IgE Abs.

36 e kinetics were identical to those caused by anti-IgE activation.

37 BAL were also significantly decreased after anti-IgE administration 24 hour and 48 hour after the la

38 these cell-signalling pathways abolished the anti-IgE/allergen-dependent MMP-9 release.

39 horylation when compared with either IL-3 or anti-IgE alone; pre-exposure to IL-3 induced a final 13-

40 d food allergy and will examine the place of anti-IgE among current therapeutic options for the treat

41 silonRIalpha surface density, and polyclonal anti-IgE and Ag-induced basophil histamine release respo

42 ause targeted biotherapeutic agents, such as anti-IgE and anti-cytokine antibodies, are becoming avai

43 CD63 peanut/anti-IgE and CD-sens values can be used to estimate the

44 il presence), and basophil HR in response to anti-IgE and formyl-methionine-leucine-phenylalanine.

45 Erk phosphorylation (6-fold above the sum of anti-IgE and IL-3 alone).

46 Blood was incubated with peanut extract or anti-IgE and tests were performed as follows: BAT-CD63 u

47 KCa1 currents following activation with both anti-IgE and the iKCa1 opener 1-EBIO, and was reversed b

48 The efficacy of omalizumab (anti-IgE) and increased IgE levels in patients with chro

49 s immunotherapy, immunotherapy combined with anti-IgE, and Chinese herbal medicine as well as approac

50 rnal and CB serum concentrations of IgE, IgG anti-IgE, and IgG anti-IgE/IgE ICs were determined in a

51 However, 5-lipoxygenase inhibitors, anti-IgE, and immunomodulatory drugs are also likely to

52 Mice were subsequently treated with anti-IgE, and the symptoms of passive IgE-mediated anaph

53 tion was also observed upon stimulation with anti-IgE, anti-FcepsilonRIalpha, IL-3, and A23187 in a d

54 e biologics include immunotherapy with novel anti-IgE antibodies and analogs, small-molecule inhibito

55 he analyte is sandwiched between immobilized anti-IgE antibodies and aptamer-bearing reporter phage m

56 Such therapies include anti-IgE antibodies and the soluble IL-4 receptor.

57 FcepsilonRI, and the therapeutic efficacy of anti-IgE antibodies imply that IgE-mediated mechanisms a

58 ct in a manner distinct from therapeutic IgG anti-IgE antibodies such as omalizumab.

59 ergen, or cross-linking anti-FcepsilonRI and anti-IgE antibodies, on surface TSLP receptor in 24-hour

60 or by a combination of anti-IgG receptor and anti-IgE antibodies.

61 A recombinant humanized monoclonal anti-IgE antibody (omalizumab) forms complexes with free

62 By using a murine anti-IgE antibody as a template, we humanized, increased

63 etermine whether the increase in response to anti-IgE antibody is a reflection of an increased cellul

64 ozymes by 1 minute, whereas stimulation with anti-IgE antibody led to no detectable changes in PKC lo

65 The effectiveness of the injectable anti-IgE antibody omalizumab has validated IgE as an imp

66 Administration of the therapeutic anti-IgE antibody omalizumab to patients induces strong

67 ntrolled OA were treated with the monoclonal anti-IgE antibody omalizumab.

68 nteraction can be blocked by the therapeutic anti-IgE antibody omalizumab.

69 directly compared them with the established anti-IgE antibody omalizumab.

70 o 96 hours with media alone, a cross-linking anti-IgE antibody or control IgG.

71 pression, and histamine release responses to anti-IgE antibody or peanut allergen) were obtained at 3

72 QGE031 is an investigational anti-IgE antibody that binds IgE with higher affinity th

73 ti-IgE) (omalizumab), a humanized monoclonal anti-IgE antibody that binds to circulating IgE, has bee

74 tration of the capacity of pretreatment with anti-IgE antibody to blunt seasonal virus-associated ast

75 By using anti-IgE antibody treatments and mice with targeted muta

76 MA) +/- ionomycin, f-met-leu-phe (FMLP), and anti-IgE antibody were examined.

77 of shc-Grb2-Sos2 following stimulation with anti-IgE antibody, but not FMLP, in human basophils.

78 Anti-IgE antibody, but not FMLP, resulted in phosphoryla

79 Omalizumab, a recombinant anti-IgE antibody, effectively treats chronic spontaneou

80 Omalizumab, a therapeutic anti-IgE antibody, has unpaired cysteine residues in the

81 Omalizumab, an anti-IgE antibody, is used to treat patients with severe

82 The efficacy of anti-IgE antibody, omalizumab, was studied in patients w

83 An anti-IgE antibody, omalizumab, which binds to circulatin

84 thermore, we demonstrated that a therapeutic anti-IgE antibody, omalizumab, which inhibits IgE bindin

85 ith peanut allergen or non-specifically with anti-IgE antibody, was strongly suppressed by active OIT

86 by selective inhibitor (LY294002) abolished anti-IgE antibody- but not FMLP-induced phosphorylation

87 lease (HR) response ex vivo to cross-linking anti-IgE antibody.

88 e in the maximal HR induced by cross-linking anti-IgE antibody.

89 Omalizumab is a widely used therapeutic anti-IgE antibody.

90 cific IgE was demonstrated using a secondary anti-IgE antibody.

91 Anti-IL-5 (TRFK-5) or anti-IgE (antibody 1-5) was administered before each air

92 Address the hypothesis that: (i) IgG anti-IgE autoantibodies are detectable in the serum of a

93 Naturally occurring IgG anti-IgE autoantibodies may inhibit, as well as induce,

94 ponders" to the Allerport(R) HRT (%HR due to anti-IgE below 20%) were excluded.

95 om LAD2 cells stimulated by either SP or IgE/anti-IgE, but only methlut and luteolin significantly in

96 ls did not produce MIP-1alpha in response to anti-IgE, but they did so in response to A23187.

97 ation with peanut and after stimulation with anti-IgE (CD63 peanut/anti-IgE) was independently associ

98 ne and lipid mediator release in response to anti-IgE challenge, both under baseline conditions and a

99 Basophils that do not degranulate after anti-IgE challenge, known as "nonreleaser" basophils, ch

100 -mediated bronchoconstriction resulting from anti-IgE challenge.

101 that a recombinant single-chain neutralizing anti-IgE could not only neutralize circulating IgE, but

102 l data for QGE031, a high-affinity IgG1kappa anti-IgE, demonstrate that increased suppression of free

103 during passive sensitization enhanced their anti-IgE-dependent histamine exocytosis and increased th

104 Therapy with anti-IgE depresses circulating free IgE to the limits of

105 immune complexes were generated with IgG(1) anti-IgE directed against the Cepsilon4 domain, the abso

106 appeared possible because both antigens and anti-IgE dissociated rapidly from cells after washing to

107 IgE treatment and has identified significant anti-IgE effects on both basophils and dendritic cells,

108 th the IgE density, and unlabeled polyclonal anti-IgE enhanced the nonuniform IgE distributions.

109 N-formyl-methionyl-leucyl-phenylalanine, or anti-IgE greatly enhanced proton currents, the latter su

110 the secretion of protein in response to IL-3/anti-IgE, had no effect on the generation of IL-13 in th

111 Recombinant monoclonal humanized anti-IgE has put forward a fundamentally new concept for

112 Clinical studies with anti-IgE have promoted and will continue to advance the

113 Nonspecific (anti-IgE), helminth-specific, and HDM-allergen-specific

114 IgG anti-IgE/IgE ICs generated in vitro bound strongly to Fc

115 Measuring maternal or CB levels of IgG anti-IgE/IgE ICs may be a more accurate predictor of all

116 concentrations of IgE, IgG anti-IgE, and IgG anti-IgE/IgE ICs were determined in a cohort of allergic

117 Maternal and CB serum concentrations of IgG anti-IgE/IgE ICs were highly correlated, regardless of m

118 as detected in solutions of transcytosed IgG anti-IgE/IgE ICs, even though essentially all the IgE re

119 g and transcytosis of IgE in the form of IgG anti-IgE/IgE ICs.

120 ithelial transport of IgE in the form of IgG anti-IgE/IgE ICs.

121 ediated transcytosis of maternal-derived IgG anti-IgE/IgE ICs.

122 IgG(1) anti-IgE/IgE immune complexes were detected in allergic

123 levels of OVA-specific antibodies and IgG(1) anti-IgE/IgE immune complexes were determined in allergi

124 e were gavage fed TNP-specific IgE as IgG(1) anti-IgE/IgE immune complexes, IgG(1) isotype control an

125 o absorb TNP-specific IgE when fed as IgG(1) anti-IgE/IgE immune complexes.

126 ransplacental passage of maternal IgE as IgG anti-IgE/IgE immune complexes.

127 sed from isolated basophils following either anti-IgE, IL-3 or fMLP stimulation.

128 esent recent data from clinical studies with anti-IgE in asthma, allergic rhinitis, and food allergy

129 ndings of the most recent clinical trials of anti-IgE in the treatment of allergic disorders are disc

130 some promising results regarding the use of anti-IgE in the treatment of other atopic diseases and a

131 table degranulation following treatment with anti-IgE in vitro.

132 ubation with IL-3 (15 min or 18 h) augmented anti-IgE-included basophil MIP-1alpha production.

133 Conversely, activating MCs with anti-IgE increased the time partition between signaling

134 vation with Ca(2+) ionophore (A23187) or IgE-anti-IgE induced eNOS phosphorylation and translocation

135 and ibrutinib were also found to counteract anti-IgE-induced and allergen-induced upregulation of CD

136 The anti-IgE-induced basophil IL-13 synthesis could be enhan

137 th both LA-heparin and fragmin inhibited the anti-IgE-induced degranulation of rat peritoneal mast-ce

138 nduced a final 13-fold average increase over anti-IgE-induced Erk phosphorylation (6-fold above the s

139 All four BTK blockers were found to inhibit anti-IgE-induced histamine release from basophils in non

140 rentuximab-vedotin was found to downregulate anti-IgE-induced histamine release in CD30(+) MCs.

141 bation (with and without IL-3 preincubation, anti-IgE-induced IL-13 production was 227 +/- 99 and 42

142 gs showed inhibition of PMA-induced, but not anti-IgE-induced, histamine release.

143 Patients with CD63 peanut/anti-IgE levels of 1.3 or greater had an increased risk

144 Previously, infusions of an anti-IgE mAb (rhumAb-E25) in subjects decreased serum Ig

145 Treatment with the anti-IgE mAb decreased free IgE levels to 1% of pretreat

146 Anti-IgE mAb has positive effects in OA induced by persu

147 examined in 15 subjects receiving humanized anti-IgE mAb intravenously.

148 The dramatic effects of the anti-IgE mAb omalizumab to lower free IgE levels and Fc

149 animals were injected intraperitoneally with anti-IgE mAb or PBS 6 hours before challenge with AP or

150 Rapid desensitization with anti-IgE mAb suppressed IgE-mediated immediate hypersens

151 In AP-sensitized and challenged mice, anti-IgE mAb treatment abolished AHR 24 hour and 48 hour

152 Anti-IgE mAb treatment almost completely neutralized fre

153 Omalizumab is a human anti-IgE mAb with proved efficacy in patients with sever

154 and biological agents, such as anti-IL-5 and anti-IgE mAb, and can be based on different biomarkers t

155 sensitized with serially increasing doses of anti-IgE mAb, anti-FcepsilonRIalpha mAb, or antigen.

156 validated by the approval of omalizumab, an anti-IgE mAb, for patients with chronic spontaneous urti

157 Omalizumab, an anti-IgE mAb, has recently been approved by the US Food

158 Omalizumab, an anti-IgE mAb, is the first targeted biologic therapeutic

159 Active and passive models of antigen- and anti-IgE mAb-induced IgE-mediated anaphylaxis were used.

160 We demonstrated that these low-affinity anti-IgE mAbs bind to the cell surface-bound IgE without

161 cations that relate to the increasing use of anti-IgE mAbs for the treatment of allergic disease.

162 profile, indicating that use of low-affinity anti-IgE mAbs holds promise as a novel therapeutic appro

163 Instead, the low-affinity anti-IgE mAbs profoundly block human peanut- and cat-all

164 This is in contrast to the high-affinity anti-IgE mAbs that trigger anaphylactic degranulation at

165 lergic reaction blockade by the low-affinity anti-IgE mAbs was correlated with their capacity to down

166 In placebo-controlled studies with anti-IgE, many patients were able to substantially reduc

167 ergic bronchoconstriction in sheep, inhibits anti-IgE mediated histamine release in isolated mast cel

168 -5 alone for 5 d with SCF minimally enhanced anti-IgE-mediated cys-LT generation, these cytokines ind

169 Similar to FMLP, PD98059 inhibited anti-IgE-mediated LTC4 release (IC50, approximately 2 mi

170 gen-induced bronchoconstriction and inhibits anti-IgE-mediated mast-cell degranulation.

171 The anti-IgE medication omalizumab (Xolair; Genentech, South

172 cepsilonRI) is extensively cross-linked with anti-IgE, molecules associated with cholesterol-rich mic

173 In this study, we evaluate whether anti-IgE monoclonal antibody (mAb) has an effect in a mo

174 In phase 2 trials, omalizumab, an anti-IgE monoclonal antibody [corrected] that targets Ig

175 e conclude that aerosol administration of an anti-IgE monoclonal antibody does not inhibit the airway

176 e effectiveness of anti-leucotrienes and the anti-IgE monoclonal antibody omalizumab in some patients

177 We conclude that an anti-IgE monoclonal antibody, which inhibits binding of

178 binant house dust mite (rDer p2) allergen or anti-IgE (n = 10).

179 L-6, and IL-13, in basophils stimulated with anti-IgE, N-formyl-methionyl-leucyl-phenylalanine, or ph

180 Treatment with an anti-IgE-neutralizing antibody fully reversed vascular i

181 We did a pilot study testing whether anti-IgE (omalizumab) combined with multifood oral immun

182 In addition, anti-IgE (omalizumab) has been shown to be safe and well

183 Anti-IgE (omalizumab) treatment ablated this anaphylacti

184 It has also become clear that anti-IgE (Omalizumab), the first monoclonal antibody reg

185 Anti-immunoglobulin E (anti-IgE) (omalizumab), a humanized monoclonal anti-IgE

186 Weak to moderate stimulation with IgE plus anti-IgE or IgE plus Ag enhances survival, while stronge

187 Stimulation with anti-IgE or IL-3 resulted in strong upregulation of baso

188 prevent cytokine secretion induced by either anti-IgE or IL-3.

189 channels, and the proton channel response to anti-IgE or PMA persisted in Ca(2+)-free solutions.

190 Mast cells were challenged with anti-IgE or SCF and the generation of histamine, cystein

191 ent using allergen avoidance, immunotherapy, anti-IgE, or antifungal treatment is an important part o

192 of FcepsilonRI with monomeric IgE, IgE plus anti-IgE, or IgE plus low Ag, Lyn (a Src family kinase)

193 emission ratioing of fluorescence approach, anti-IgE produced acidification that was exacerbated in

194 Anti-IgE reduces the expression of FcepsilonRI on inflam

195 An unrelated challenge (birch, rDer p2 or anti-IgE) resulted in 53.4% activation (30.8-66.8, P = 0

196 Therapeutic anti-IgE stimulated a calcium response in primary B cell

197 tic subjects that establish higher basal and anti-IgE-stimulated basophil degranulation among the ast

198 was not changed by IL-3 priming, IL-3-primed anti-IgE-stimulated basophils showed a strong synergism

199 ion for 5 d with IgE in the presence of SCF, anti-IgE-stimulated hMCs elaborated minimal cys-LT (0.1

200 The anti-IgE-stimulated response occurred in a fraction of c

201 solated monocytes did not release MMP-9 upon anti-IgE stimulation, but MMP-9 release was induced by s

202 s calcium/magnesium was added at the time of anti-IgE stimulation.

203 s was significantly induced in mast cells by anti-IgE stimulation.

204 6 suppressed production of all chemokines by anti-IgE stimulation.

205 the same donors did not release IL-13 after anti-IgE stimulation.

206 es (84%) were not upregulated after a single anti-IgE stimulus, indicating a significantly different

207 ly induced with concentrations of antigen or anti-IgE that were suboptimal for secretion.

208 psilonRI binding have been identified and an anti-IgE therapeutic antibody (omalizumab) is used to tr

209 epsilonRII), but in contrast, binding of the anti-IgE therapeutic antibody omalizumab decreases the e

210 for the optimal design of safe and effective anti-IgE therapies and suggest that the IgE memory B cel

211 acerbations was demonstrated and improved by anti-IgE therapy (omalizumab).

212 research that has led to the development of anti-IgE therapy and other strategies targeting IgE and

213 Control Evaluation study and the Inner City Anti-IgE Therapy for Asthma study.

214 CASI was validated by using the Inner City Anti-IgE Therapy for Asthma trial.

215 Omalizumab is an established anti-IgE therapy for the treatment of allergic diseases

216 Studies of anti-IgE therapy have significantly advanced our underst

217 Anti-IgE therapy in allergic asthma has been evaluated m

218 gic diseases was obtained by the efficacy of anti-IgE therapy in many clinical trials on asthma and o

219 erscores the short- and long-term benefit of anti-IgE therapy in terms of the following: improving lu

220 Anti-IgE therapy is beneficial in selected patients with

221 d be used for total control of symptoms; and anti-IgE therapy is newly licensed in the USA.

222 The injectable anti-IgE therapy omalizumab has been shown to benefit in

223 year saw encouraging reports on omalizumab (anti-IgE therapy) in severe allergic asthma, by Stephen

224 Prospective (anti-IgE therapy, adenosine receptor antagonists, phosph

225 This article reviews current concepts of anti-IgE therapy, with a focus on recent studies that pr

226 ith budesonide and formoterol fumarate), and anti-IgE therapy.

227 tological analysis of the lung sections from anti-IgE-treated mice revealed normal inflammatory patte

228 Anti-IgE-treated mice showed a significant improvement i

229 Interestingly, upon subsequent challenge of anti-IgE-treated mice with an IgE cross-linking reagent

230 s into the kinetics of cellular responses to anti-IgE treatment and has identified significant anti-I

231 hocytes, and interleukin-4-positive cells by anti-IgE treatment and has provided insight into the mec

232 monitor patients on allergen immunotherapy, anti-IgE treatment or in the natural resolution of aller

233 Anti-IgE treatment significantly decreased serum anti-OV

234 nt for therapeutic decisions (eg, the use of anti-IgE treatment).

235 g mast cell depletion (with anti-c-kit mAb), anti-IgE treatment, and Fc epsilon RI-deficient mice ind

236 s in patients with severe disease undergoing anti-IgE treatment.

237 lap between genes upregulated after repeated anti-IgE triggering and genes upregulated in tissue from

238 changes in mast cell function after repeated anti-IgE triggering.

239 adherence (2.54, 0.97-6.67-borderline), and anti-IgE use in a protective way (0.26, 0.12-0.53).

240 57% of non-CIU subjects (n=23), whereas IgG anti-IgE was present in 43% of CIU-R, 45% of CIU-NR, and

241 Induction of CCL2, CCL7, CXCL3, and CXCL8 by anti-IgE was significantly inhibited by dexamethasone bu

242 after stimulation with anti-IgE (CD63 peanut/anti-IgE) was independently associated with severity (P

243 Basophils in medium alone or with IL-3 +/- anti-IgE were coincubated with TSLP, IL-33, or IL-25.

244 Finally, new therapeutic applications of anti-IgE were identified.

245 -in milk if they tolerate it, and the use of anti-IgE with or without concomitant immunotherapy.

246 were stimulated with substance P (SP) or IgE/anti-IgE with or without preincubation with luteolin, me