ライフサイエンスコーパス: FcepsilonRI

1 pressing the high-affinity receptor for IgE (FcepsilonRI).

2 ltaneously promotes allergic stimulation via FcepsilonRI.

3 olism in response to stimulation through the FcepsilonRI.

4 l factor, whereas the opposite was found for FcepsilonRI.

5 Rs decrease ability to indirectly cross-link FcepsilonRI.

6 r protection was mostly lost in mice lacking FcepsilonRI.

7 mast cells and express CD117, tryptase, and FcepsilonRI.

8 ton in regulating functional interactions of FcepsilonRI.

9 s expressing the high-affinity IgE receptor, FcepsilonRI.

10 iators upon antigen-driven engagement of the FcepsilonRI.

11 basophilic cell line stably expressing human FcepsilonRI.

12 xpression of the high-affinity IgE receptor, FcepsilonRI.

13 sident cells via its high-affinity receptor, FcepsilonRI.

14 ceptors such as tetrameric (alphabetagamma2) FcepsilonRI.

15 ression in human basophils is aggregation of FcepsilonRI.

16 FcepsilonRI-activated cells with Gal3 knockdown exhibite

17 onRI cross-linking by antigen-IgE complexes (FcepsilonRI-activated mast cells [FcepsilonRI-MCs]).

18 ses, such as carboxypeptidase A, released by FcepsilonRI-activated MCs detoxify an increasing number

19 FcepsilonRI-activated MCs upregulated NK1R and HK-1 tran

20 imply that therapeutic targeting of the IgE/FcepsilonRI activation cascade will not affect sensitiza

21 a noncanonical function in antigen dependent-FcepsilonRI activation in mast cells.

22 Following FcepsilonRI activation, nonoxidized rather than oxidized

23 ey associated with the plasma membrane after FcepsilonRI activation.

24 Responses to FcepsilonRI aggregation and expression of proteases and

25 ergic mast cell (MC) degranulation occurs by FcepsilonRI aggregation and varies in strength among sub

26 y induced on mouse and human mast cells upon FcepsilonRI aggregation but its functional effects are u

27 MC priming was particularly pronounced when FcepsilonRI aggregation was in the suboptimal range, ref

28 itivity ( approximately 50-fold) of cells to FcepsilonRI aggregation with enhancement of degranulatio

29 lation with MRGPRX2 agonists (but not C3a or FcepsilonRI aggregation) resulted in refractoriness to f

30 liferation, maturation, and reactivity after FcepsilonRI aggregation.

31 ) cells and examined for releasability after FcepsilonRI aggregation.

32 by compound 48/80 or substance P but not by FcepsilonRI aggregation.

33 h flow cytometry, and in vivo by using human FcepsilonRI alpha-chain transgenic mice in a functional

34 ous anaphylaxis in mice expressing the human FcepsilonRI alpha-chain.

35 y, omalizumab, which inhibits IgE binding to FcepsilonRI, also inhibited IgE binding to CD23.

36 lso accelerates the dissociation of IgE from FcepsilonRI, although much less efficiently than E2_79.

37 e effects of allergen, or cross-linking anti-FcepsilonRI and anti-IgE antibodies, on surface TSLP rec

38 -dependent suppression of free IgE, basophil FcepsilonRI and basophil surface IgE superior in extent

39 identified a functional interaction between FcepsilonRI and CD13 in murine MCs.

40 dicative of a functional interaction between FcepsilonRI and CD13 on MCs.

41 h are mediated through its two Fc receptors, FcepsilonRI and CD23 (FcepsilonRII).

42 functions principally through two receptors, FcepsilonRI and CD23 (FcepsilonRII).

43 The conformational changes associated with FcepsilonRI and CD23 binding to IgE-Fc ensure that their

44 Simultaneous binding of IgE to FcepsilonRI and CD23 is blocked by reciprocal allosteric

45 mplexes (IgE-ICs) target the 2 IgE receptors FcepsilonRI and CD23, and we investigated the functional

46 ion and two principal cell surface receptors FcepsilonRI and CD23.

47 Coligation of FcepsilonRI and CD300c increased intracellular calcium m

48 ucing activity of IgG autoantibodies against FcepsilonRI and IgE, reducing activity of IgE autoantibo

49 eral blood basophils (n=60) to specific anti-FcepsilonRI and IgE-independent fMLP stimulation was det

50 autologous serum skin test (ASST); IgG anti-FcepsilonRI and IgG anti-IgE; IgG-anti-thyroperoxidase (

51 nalysis to measure the codistribution of IgE-FcepsilonRI and Lyn on the plasma membrane of fixed cell

52 We found that Syk colocalizes transiently to FcepsilonRI and that Syk-FcepsilonRI binding dynamics ar

53 E antibodies that bind to mast cells through FcepsilonRI and trigger immediate hypersensitivity react

54 dy shows that AhR activation by FICZ reduces FcepsilonRI and upregulates IDO expression in LC.

55 gE (bound to high-affinity surface receptors FcepsilonRI) and stimulated using the antigen DNP-BSA.

56 155 and PU.1 (as upstream regulatory axis of FcepsilonRI) and transcription factors Elf-1 and YY1.

57 ase enzyme targeted towards the IgE receptor FcepsilonRI, and administering asialylated IgE-markedly

58 tion and calcium responses downstream of the FcepsilonRI, and agents that relieve actin reorganizatio

59 D) carry the high-affinity receptor for IgE, FcepsilonRI, and are crucially involved in the pathogene

60 E antibodies, the high-affinity IgE receptor FcepsilonRI, and mast cells can contribute toward acquir

61 autoantibodies against IgE or its receptor, FcepsilonRI, and the therapeutic efficacy of anti-IgE an

62 robustly the high-affinity receptor for IgE, FcepsilonRI, and thereby sense allergens.

63 ariability is comparable between the routes, FcepsilonRI- and MRGPRX2-stimulated pathways are complet

64 ith anti-FcepsilonRI antibody [%CD63(+)/anti-FcepsilonRI], and area under the dose-response curve [AU

65 D63(+) basophils after stimulation with anti-FcepsilonRI antibody [%CD63(+)/anti-FcepsilonRI], and ar

66 ta1- and beta3-integrins colocalize with IgE-FcepsilonRI at patterned ligand surfaces as cells spread

67 ,25(OH)(2)-D(3)] significantly downregulated FcepsilonRI at the protein and mRNA levels of the recept

68 ing compared with activation through the IgE/FcepsilonRI axis alone.

69 shows superior inhibition of IgE binding to FcepsilonRI, basophil activation, IgE production by B ce

70 -ICs were noninflammatory because of reduced FcepsilonRI binding and enhanced CD23-dependent serum cl

71 izes transiently to FcepsilonRI and that Syk-FcepsilonRI binding dynamics are independent of receptor

72 opose that the Lin(-) CD34(hi) CD117(int/hi) FcepsilonRI(+) blood cells are closely related to human

73 Isolated Lin(-) CD34(hi) CD117(int/hi) FcepsilonRI(+) blood cells had an immature mast cell-lik

74 r frequency of Lin(-) CD34(hi) CD117(int/hi) FcepsilonRI(+) blood mast cell progenitors than asthmati

75 ophil activation by antigen cross-linking of FcepsilonRI-bound IgE is central to allergy pathogenesis

76 as the ability to co-ligate FcgammaRIIB with FcepsilonRI-bound IgE on allergic effector cells and rep

77 ule simultaneously targeting FcgammaRIIB and FcepsilonRI-bound IgE on the surface of allergic effecto

78 IgG autoantibodies binding to both free and FcepsilonRI-bound IgE were detected in patients with ato

79 , and propose that 'free' SPE-7 IgE binds to FcepsilonRI-bound SPE-7 IgE by an Fv-Fv interaction.

80 b region of 'free' SPE-7 IgE with the Fab of FcepsilonRI-bound SPE-7 IgE is the basis of its cytokine

81 oninflammatory through reduced engagement by FcepsilonRI but increased targeting of the CD23 pathway.

82 t that constitutive internalization of human FcepsilonRI by DCs and monocytes distinctively contribut

83 the IgE-bound, high-affinity IgE receptors (FcepsilonRI) by allergens or Ags and the binding of anap

84 of the receptor for immunoglobulin E (IgE), FcepsilonRI, by Lyn kinase after IgE-FcepsilonRI complex

85 Activated mast cell MPs (CD137(+) FcepsilonRI(+)c-kit(+)MPs) were significantly increased

86 , mast cell MPs (high-affinity IgE receptor [FcepsilonRI](+)c-kit(+)MPs), and basophil MPs (CD203c(+)

87 FcepsilonRI(+) cells were found in the human renal corte

88 y to assess the distribution and function of FcepsilonRI+ cells.

89 ompanied by augmented phosphorylation within FcepsilonRI clusters.

90 Allergen cross-linking of the IgE/FcepsilonRI complex activates these cells, inducing rele

91 IgE-FcepsilonRI complex dissociation was analyzed in vitro b

92 cells via driving internalization of the IgE/FcepsilonRI complex.

93 Ag-mediated crosslinking of IgE-FcepsilonRI complexes activates mast cells and basophils

94 (IgE), FcepsilonRI, by Lyn kinase after IgE-FcepsilonRI complexes are cross-linked by multivalent an

95 ion was elicited when approximately 2700 IgE-FcepsilonRI complexes were occupied with specific IgE an

96 mpete with intact Pen a 1 for binding to IgE-FcepsilonRI complexes, and represent a starting point fo

97 exceptionally slow dissociation rate of IgE-FcepsilonRI complexes, such allergic effector cells perm

98 ramework regions to SEEs in SEE-anti-SEE IgE-FcepsilonRI complexes.

99 work regions of anti-SEE IgE in anti-SEE IgE-FcepsilonRI complexes.

100 ow that Gal3 promotes internalization of IgE-FcepsilonRI complexes; this may be related to our findin

101 , FcRgamma, and, to a lesser extent, IgE and FcepsilonRI contribute to effective immunity in primary

102 ffinity, non-cross-linking natural ligand of FcepsilonRI, could be used to target Ags to DCs and to i

103 w-derived mast cells (MC) were stimulated by FcepsilonRI cross-linking and release of sFcepsilonRI wa

104 opic disorders, secreting TNF and IL-6 after FcepsilonRI cross-linking by antigen-IgE complexes (Fcep

105 after activation with different stimuli, by FcepsilonRI cross-linking or by stimulation with hymenop

106 binding to FcepsilonRI on mast cells without FcepsilonRI cross-linking, can promote the proliferation

107 A significant reduction in FcepsilonRI cross-linking-mediated surface expression of

108 vels by regulating exocytosis independent of FcepsilonRI cross-linking.

109 of inflammatory CD88(-)CD14(+)CD1c(+)CD163(+)FcepsilonRI(+) DCs.

110 rough promoting IgG1-mediated damping of the FcepsilonRI-dependent acute-phase reaction.

111 r understanding the efficient suppression of FcepsilonRI-dependent allergic reactions by ligelizumab

112 Constitutive and FcepsilonRI-dependent HLMC histamine release, HASMC cont

113 Inhibition of FcepsilonRI-dependent HLMC mediator release by beta2-ago

114 linking of CD13 causes IL-6 production in an FcepsilonRI-dependent manner.

115 t for cell-to-cell contact, aggregation, and FcepsilonRI-dependent signaling.

116 at acts as a positive regulator in mast cell FcepsilonRI-dependent signaling.

117 argeted mast cells inhibits antigen-induced, FcepsilonRI-dependent spleen tyrosine kinase (Syk) phosp

118 AhR-mediated regulation of FcepsilonRI did not involve any known transcription fact

119 lishes that functional autoantibodies to IgE/FcepsilonRI do not provide a good explanation for the va

120 In contrast, COX-1 was dispensable for FcepsilonRI-driven CysLT production.

121 activation of the high-affinity IgE receptor FcepsilonRI elicits release of mast-cell renin.

122 resulted in impaired activation of IDEC upon FcepsilonRI engagement as monitored by CD83 expression.

123 IgE and FcepsilonRI engagement can also decrease the release thr

124 Furthermore, IgE-FcepsilonRI engagement potentiates the ability of mast c

125 ve oxygen species levels were measured after FcepsilonRI engagement.

126 Here, we found that FcepsilonRI expressed by human blood DC antigen 1-positi

127 mans; however, the specific functions of the FcepsilonRI expressed by these cells are not completely

128 We hypothesized that vitamin D(3) impacts FcepsilonRI expression and addressed this in human ex vi

129 0 promotes the down-regulation of MC surface FcepsilonRI expression and leads to desensitization of m

130 izumab on clinical efficacy, IgE levels, and FcepsilonRI expression in a clinical model of allergic a

131 FcepsilonRI expression in basophils was required for the

132 We show that vitamin D(3) directly reduces FcepsilonRI expression on dendritic cells by inhibiting

133 d intestinal allergy occurred independent of FcepsilonRI expression on mast cells (MCs) and basophils

134 val, and activation of mast cells; increased FcepsilonRI expression on mast cells; and enhanced the p

135 which was associated with recapitulation of FcepsilonRI expression on the MCs.

136 liminate surface high-affinity IgE receptor (FcepsilonRI) expression and function, rendering mast cel

137 nse to anti-IgE Abs, and agonist Abs against FcepsilonRI, FcepsilonRII/CD23 and galectin-3.

138 In addition, immunoglobulin receptor (FcepsilonRI, FcgammaRII) expression and surface bound an

139 cells, IgG, and FcRgamma>mast cells>IgE and FcepsilonRI>basophils.

140 mice independently of the IgE-Fc epsilon RI (FcepsilonRI)-histamine axis.

141 tor release by ambient air was determined in FcepsilonRI-humanized basophils.

142 25%) were BASO+, and 105 (58%) were IgG anti-FcepsilonRI+/IgE+.

143 her patients make IgG autoantibodies against FcepsilonRI, IgE, or both, which might chronically activ

144 mains to phosphorylated tyrosines within the FcepsilonRI immunoreceptor tyrosine-based activation mot

145 oskeleton and its continued association with FcepsilonRI impede the capacity of desensitized MCs to e

146 ation of LC by FICZ caused downregulation of FcepsilonRI in CD34LC without affecting their maturation

147 Furthermore, cross-linking of mast-cell FcepsilonRI in ex vivo murine hearts passively sensitize

148 uding integrins, to regions of clustered IgE-FcepsilonRI in processes that depend on stimulated actin

149 e role of the high-affinity IgE Fc receptor (FcepsilonRI) in allergic sensitization was evaluated usi

150 ation of the high-affinity receptor for IgE (FcepsilonRI) in mast cells initiates activation events t

151 ream signaling mediated by the IgE receptor (FcepsilonRI) in RBL mast cells utilizing surface-pattern

152 member IL-33R mediates Fcepsilon-receptor-I (FcepsilonRI)-independent activation of mast cells leadin

153 f mTOR by short hairpin RNA had no impact on FcepsilonRI-induced degranulation, whereas downregulatio

154 elieve actin reorganization rescue mast cell FcepsilonRI-induced degranulation.

155 Classical FcepsilonRI-induced mast cell (MC) activation causes syn

156 However, FcepsilonRI-induced mast cell degranulation was unaffect

157 IL-33 enhances FcepsilonRI-induced mediator release in human basophils

158 bodies to IgE or its high-affinity receptor (FcepsilonRI) induces mast cell degranulation and subsequ

159 f5b did not affect cytokine secretion, early FcepsilonRI-initiated signaling pathways, or microtubule

160 signaling pathway occurs at the level of Syk-FcepsilonRI interactions, with key outcomes dependent up

161 FcepsilonRI is also constitutively expressed in dendriti

162 The high-affinity IgE receptor FcepsilonRI is constitutively expressed in mast cells an

163 The interaction with FcepsilonRI is primarily responsible for allergic sensit

164 regation of high-affinity receptors for IgE (FcepsilonRI) is negatively regulated by rictor independe

165 capacity to downregulate the surface IgE and FcepsilonRI level on human basophils and the human Fceps

166 late-phase cytokine production downstream of FcepsilonRI ligation.

167 on of signaling intermediates evoked only by FcepsilonRI ligation.

168 reatment of helminth-infected mice with anti-FcepsilonRI mAb, a protocol known to deplete basophils,

169 lyses have identified a central role for IgE/FcepsilonRI/mast cells in promoting IgE-mediated anaphyl

170 es of SP and HK-1 as potential adjuvants for FcepsilonRI-MC-mediated allergic disorders.

171 ovide adjuvancy for efficient development of FcepsilonRI-MC-mediated disorders.

172 MMCs were used to evaluate NK1R signaling on FcepsilonRI-MC-mediated passive local and systemic anaph

173 esting an adjuvant role for NK1R agonists in FcepsilonRI-MC-mediated pathologies; however, in-depth r

174 addition to the high-affinity IgE receptor (FcepsilonRI), MCs express numerous G protein-coupled rec

175 investigate the effects of NK1R signaling on FcepsilonRI-MCs.

176 complexes (FcepsilonRI-activated mast cells [FcepsilonRI-MCs]).

177 (2019) show that the receptors MRGPRB2 and FcepsilonRI mediate distinct types of mast cell activati

178 ined that mast cells are activated via a non-FcepsilonRI mediated response following silver nanoparti

179 nnective tissue-like mast cell survival upon FcepsilonRI-mediated activation in vitro.

180 st cell functions including development, IgE:FcepsilonRI-mediated activation, and responses to food a

181 modulation of mast cell function on repeated FcepsilonRI-mediated activation.

182 llergen binding to B cells but also enhanced FcepsilonRI-mediated allergen-driven basophil activation

183 E, gamma-tocopherol (gammaT), could suppress FcepsilonRI-mediated basophil activation.

184 n, and survival, miR-155 deficiency enhances FcepsilonRI-mediated degranulation and release of TNF-al

185 tional signaling regulator that can regulate FcepsilonRI-mediated degranulation independently of mTOR

186 EP2 and EP4 agonism also curbed FcepsilonRI-mediated degranulation of human MCs.

187 brin(-/-) mast cells also exhibit defects in FcepsilonRI-mediated degranulation.

188 ctor, in contrast with knockdown, suppressed FcepsilonRI-mediated degranulation.

189 , mast cell recruitment in vivo, and maximal FcepsilonRI-mediated mast cell activation in vitro.

190 amily are recently emerging as modulators of FcepsilonRI-mediated mast cell activation; however, mech

191 ecific for 144 selected genes for effects on FcepsilonRI-mediated mast cell degranulation and identif

192 protein beta-arrestin2 inhibits Mrgprb2 and FcepsilonRI-mediated mast cell degranulation to attenuat

193 dies, we found that PLD1 deficiency impaired FcepsilonRI-mediated mast cell degranulation; however, P

194 FcepsilonRI-mediated mast-cell renin release was inhibit

195 In fact, FcepsilonRI-mediated MC histamine release was synergisti

196 uggest that miR-155 plays a critical role in FcepsilonRI-mediated MC responses by modulating componen

197 that produce characteristics concordant with FcepsilonRI-mediated secretion was zero in 34 subjects w

198 te that PLD1 and PLD2 play positive roles in FcepsilonRI-mediated signaling and mast cell function.

199 in both positive and negative regulation of FcepsilonRI-mediated signaling events in mast cells.

200 ted DEGs were significantly enriched in the "FcepsilonRI-mediated signaling pathway", while down-regu

201 prevent anaphylaxis in humans by inhibiting FcepsilonRI-mediated signaling.

202 s BTK, SYK, and LAT, critical transducers of FcepsilonRI-mediated signals that are essential for mast

203 Both plasmacytoid and IgE(+)FcepsilonRI(+) myeloid dendritic cells were present in B

204 nRI stimulation, whereas the others had anti-FcepsilonRI nonreactive basophils.

205 es of receptor aggregation kinetics based on FcepsilonRI occupancy with IgE and allergen dose.

206 hat degranulation is linked to the number of FcepsilonRI occupied with allergen-specific IgE, as well

207 domains (Syk-Y130E) led to an increased Syk-FcepsilonRI off-rate, loss of site-specific Syk autophos

208 IgE initiated allergic inflammation through FcepsilonRI on allergic effector cells, while IgE-ICs we

209 n-specific IgE to its high-affinity receptor FcepsilonRI on basophils and mast cells is a central eve

210 ction of IgE with its high-affinity receptor FcepsilonRI on basophils and mast cells is critical for

211 Furthermore, IgE bound to FcepsilonRI on BDCA1+ DCs was rapidly endocytosed, trans

212 eatures for both pattern types, IgE bound to FcepsilonRI on cells shows distinctive distributions: un

213 Thus, targeting FcepsilonRI on DCs via Ag-Fcepsilon fusion protein may s

214 ind and cross-link IgE bound to its receptor FcepsilonRI on effector cells, resulting in cell degranu

215 ch sensitizes the high-affinity IgE receptor FcepsilonRI on mast cells and basophils and drives aller

216 IgE bound to the high-affinity IgE receptor FcepsilonRI on mast cells and basophils.

217 g evidence has shown that IgE, by binding to FcepsilonRI on mast cells without FcepsilonRI cross-link

218 L-10 levels, decreased surface expression of FcepsilonRI on MCs and loss of sensitivity to IgE activa

219 , Ca(2+) -mobilization and the expression of FcepsilonRI on peritoneal MCs were quantitated.

220 Cross-linking of FcepsilonRI on the surface of mature bone marrow-derived

221 ed through both high-affinity IgE receptors (FcepsilonRI) on mast cells and basophils and low-affinit

222 patients with CSU tested that contained anti-FcepsilonRI or anti-IgE antibodies, these antibodies wer

223 ensitivity to various stimuli through either FcepsilonRI or other receptors for the degranulation pro

224 73), dendritic cell infiltrates (CD1b(+) and FcepsilonRI(+), P < .05) decreased with age.

225 secretion, and early signaling events in the FcepsilonRI pathway, including protein kinase phosphoryl

226 FLM experiments captured stimulation-induced FcepsilonRI phosphorylation and colocalization of a satu

227 Activation of mast cells through FcepsilonRI plays an important role in acute allergic re

228 We demonstrate that FcepsilonRI preferentially binds free IgE and CD23 prefe

229 cules merely sensitise mast cells by binding FcepsilonRI prior to cross-linking by multivalent allerg

230 age-negative (Lin(-)) CD34(hi) CD117(int/hi) FcepsilonRI(+) progenitor cells, which represented only

231 ptors and IgE via internalization of the IgE/FcepsilonRI, promoted a partial mediator depletion pathw

232 These distributions of IgE-FcepsilonRI propagate to the spatial recruitment of earl

233 t allergen concentrations, the %CD63(+)/anti-FcepsilonRI ratio across most allergen concentrations, t

234 The %CD63(+)/anti-FcepsilonRI ratio for all allergens and AUCs for pork ki

235 on requires direct ligation to an activating FcepsilonRI receptor.

236 ies revealed that LARI downregulated surface FcepsilonRI receptors and IgE via internalization of the

237 IgE, which lowers free IgE levels and causes FcepsilonRI receptors on basophils and mast cells to be

238 1,25(OH)(2)-D(3)-mediated FcepsilonRI reduction was direct and resulted in impaire

239 FcepsilonRI regulation by 1,25(OH)(2)-D(3) was independe

240 Comprehensive knowledge of FcepsilonRI regulation is thus required.

241 t cell activation, with an emphasis on novel FcepsilonRI regulators, immunoglobulin E (IgE)-independe

242 ndary structure and abrogated IgE binding to FcepsilonRI, rendering IgE incapable of eliciting mast c

243 ith rat basophils transfected with the human FcepsilonRI, respectively.

244 sslinking of the high-affinity IgE receptor (FcepsilonRI) resulted in genome-wide reorganization of t

245 Antigen-triggered activation of IgE-loaded FcepsilonRI results in cocapping and cointernalization o

246 IgE-mediated cross-linking of FcepsilonRI results in the release of mediators stored i

247 aphylaxis (PSA) induced HDAC3 expression and FcepsilonRI signaling in BALB/c mice.

248 om B16F10 cultures induced the activation of FcepsilonRI signaling in lung mast cells in an HDAC3-dep

249 e findings extend previous evidence that IgE-FcepsilonRI signaling is initiated by colocalization wit

250 Mast-cell-targeted genetic deletion of the FcepsilonRI signaling kinase Syk or Syk blockade also pr

251 ropose that kinetic discrimination along the FcepsilonRI signaling pathway occurs at the level of Syk

252 Fluvastatin selectively suppressed key FcepsilonRI signaling pathways, including Akt and ERK.

253 unctioned as a partial antagonist to inhibit FcepsilonRI signaling phosphorylation of Syk, Akt, Erk,

254 IL-10 enhanced activation of the key FcepsilonRI signaling proteins Stat5, JNK, and ERK.

255 FcepsilonRI signaling was observed in lung tumors derive

256 be essential for high-affinity IgE receptor (FcepsilonRI) signaling in human cells.

257 In the inflamed skin, IgE/FcepsilonRI-signalling in basophils promotes epithelial

258 igration by IL-8 or prostaglandin E(2) or to FcepsilonRI-stimulated secretion.

259 Ex vivo, FcepsilonRI stimulation of bone marrow-derived mast cell

260 FcepsilonRI stimulation of MCs promotes autocrine secret

261 ating mast cells was graded according to the FcepsilonRI stimulation strength, whereas the magnitude

262 ly impaired in cytokine production following FcepsilonRI stimulation, indicating that MALT1 scaffoldi

263 Compared with IgE-FcepsilonRI stimulation, Mrgprb2 activation of mast cell

264 e subgroup of patients' basophils reacted to FcepsilonRI stimulation, whereas the others had anti-Fce

265 pathways, or microtubule reorganization upon FcepsilonRI stimulation.

266 ase between WT and Fn14(-/-) BMMCs after IgE-FcepsilonRI stimulation.

267 HERF1 regulates mast cell response following FcepsilonRI stimulation.

268 lized to the nucleus of mast cells following FcepsilonRI stimulation.

269 ent for IL-10 in LPS-mediated decrease in MC FcepsilonRI surface expression.

270 armacologic approaches, we show that the IgE/FcepsilonRI/Syk signaling axis is critical for the devel

271 cellular infiltration (CD3(+), CD11c(+), and FcepsilonRI(+)) than adults with AD.

272 s-linking of IgE bound to the alpha chain of FcepsilonRI, the mast cell/basophil high affinity IgE re

273 sms (ie, the high-affinity receptor for IgE [FcepsilonRI]), the stem cell factor receptor KIT, the IL

274 tively promotes the dissociation of IgE from FcepsilonRI through a molecular mechanism termed facilit

275 pro-inflammatory responses downstream of IgE/FcepsilonRI, TLRs, IL-1R, and IL-33R.

276 mice, but not mice lacking IgE or functional FcepsilonRI, to survive challenge with a potentially let

277 FcepsilonRI-transfected human cell lines (MelJuso), huma

278 Moreover, we show that Rab5 is essential for FcepsilonRI-triggered association of the SNARE protein S

279 FcepsilonRI-triggered mediator release was determined in

280 and enhances cell migration while inhibiting FcepsilonRI-triggered secretion.

281 changes in mast cell function after repeated FcepsilonRI triggering and to correlate these changes to

282 ergic inflammation or the effect of repeated FcepsilonRI triggering occurring in such responses.

283 dividual variability in skin MC responses to FcepsilonRI triggering vs those evoked by MRGPRX2.

284 an all-or-none response of mast cells after FcepsilonRI triggering.

285 Cross-linking of immunoglobulin E-bound FcepsilonRI triggers multiple cellular responses, includ

286 oss-linking of mast cell (MC) IgE receptors (FcepsilonRI) triggers degranulation of secretory granule

287 finding that Gal3 is a positive regulator of FcepsilonRI ubiquitination.

288 f IgE-bound high-affinity receptors for IgE (FcepsilonRI) underlies type I allergy and anaphylactic s

289 emonstrates that the MAR-1 antibody to mouse FcepsilonRI unexpectedly binds to two Fcgamma receptors,

290 through an ITAM-containing receptor for IgE (FcepsilonRI), using signaling pathways analogous to thos

291 following DS, the high-affinity IgE receptor FcepsilonRI was still capable of transducing signals in

292 Stimulating CU patients' basophils via FcepsilonRI, we identified three distinct immunologic ph

293 ponses were achieved when only a few hundred FcepsilonRI were occupied.

294 leukemia (RBL)-SX38 cells that express human FcepsilonRI were treated with or without gammaT, followe

295 ly events in mast cell signaling mediated by FcepsilonRI where the plasma membrane is composed of man

296 sophils express high-affinity IgE receptors (FcepsilonRI), which play an essential role in allergic d

297 e for DJ-1 in the early activation of Lyn by FcepsilonRI, which is essential for human MC responses a

298 these agents enhanced colocalization of IgE-FcepsilonRI with Lyn and its saturated lipid anchor at e

299 affinity immunoglobulin E receptor-positive [FcepsilonRI+]), with an immature MC-like appearance, whi

300 e directly visualized Lyn recruitment to IgE-FcepsilonRI within 1 min of antigen stimulation.