ライフサイエンスコーパス: basophil

1 thy displayed enhanced expression of CD69 on basophils.

2 e of modulating SYK expression in developing basophils.

3 through direct interaction of IgG with human basophils.

4 g in a patient-dependent ability to activate basophils.

5 IgE (sIgE) on the surface of mast cells and basophils.

6 nd innate immune cells such as monocytes and basophils.

7 mature human tissue-resident mast cells and basophils.

8 nophil numbers, we cannot exclude a role for basophils.

9 ment of the percentage of CD63(hi) activated basophils.

10 and FcRgamma>mast cells>IgE and FcepsilonRI>basophils.

11 would weakly upregulate CD203c expression on basophils.

12 antibodies on the surface of mast cells and basophils.

13 ion of effector cells such as mast cells and basophils.

14 or IgE-mediated activation of mast cells and basophils.

15 hils, and eosinophils but not lymphocytes or basophils.

16 pon cross-linking allergens on mast cells or basophils.

17 utrophils (59.03%), eosinophils (2.84%), and basophils (71.88%).

18 ysis and quantification of ex vivo-activated basophils (according to the basophil activation test [BA

19 rved in the MCTD-like mouse model along with basophil accumulation in lymph nodes and lungs.

20 11%; P<.001), eNO (86 vs 53 ppb; P<.05) and basophil activation after 2 weeks (CD63 expression 79% v

21 nhanced FcepsilonRI-mediated allergen-driven basophil activation and histamine release.

22 Basophil activation and IgE anti-U1 small nuclear ribonu

23 immune responses that included IgE-dependent basophil activation and measurement of serum inhibitory

24 Assessments of peanut-induced basophil activation and peanut-specific immunoglobulins

25 , combined therapeutic approaches that block basophil activation and reduce eosinophil numbers could

26 Basophil activation and T-cell proliferation were tested

27 Basophil activation assays were also conducted.

28 e found between high- and low-dose groups in basophil activation at the time of desensitization or su

29 or grass pollen allergens and able to elicit basophil activation at very low allergen concentrations.

30 Mast cell and basophil activation by antigen cross-linking of Fcepsilo

31 Similarly, basophil activation by ASNase ICs depended on the antige

32 Basophil activation by unfolded mutant Ara h 2 was low (

33 Basophil activation could provide a functional surrogate

34 test wheals, peanut-specific IgE levels, and basophil activation decreased significantly, and peanut-

35 Egg white-specific IgE, skin testing, and basophil activation decreased similarly after BE and egg

36 f active OIT exhibited higher peanut-induced basophil activation ex vivo and higher peanut sIgE level

37 Basophil activation following peanut stimulation was dec

38 Combining both results led to an increase in basophil activation in 69% of patients, and only in 12%

39 lpha-gal-containing allergens induced strong basophil activation in a dose-dependent manner in patien

40 patients in an in vitro assay and inhibited basophil activation in an allergic patient ex vivo analy

41 lly measured, before, during, and after OIT, basophil activation in whole blood ex vivo in response t

42 We evaluated whether basophil activation in whole blood, and plasma levels of

43 Therefore, different aspects of basophil activation might be useful for monitoring of OI

44 ophils and their implication in IgE-mediated basophil activation processes.

45 IgG4 to IgE ratio and lower Ara h 2 IgE and basophil activation responses were associated with susta

46 Basophil activation status and the presence of autoreact

47 gE; and basophil reactivity (BASO) using the basophil activation test (BAT) and basophil histamine re

48 ristics but also diagnostic performance of a basophil activation test (BAT) and sIgG4 in nsLTP-sensit

49 tion study participants by administering the basophil activation test (BAT) and the skin prick test (

50 evaluate the usefulness of in vivo tests and basophil activation test (BAT) for the diagnosis of IHRs

51 A basophil activation test (BAT) with seasonal and/or pere

52 and/or indirectly via positive responses in basophil activation test (BAT).

53 In addition to routine diagnostics, a basophil activation test (Flow CAST) with different conc

54 x vivo-activated basophils (according to the basophil activation test [BAT]) might meet this requirem

55 Basophil activation test can predict allergic clinical s

56 dependent fMLP stimulation was determined by basophil activation test in comparison with patients suf

57 acy may come from cellular tests such as the basophil activation test or mast cell approaches.

58 The basophil activation test should be considered as an addi

59 Next, a basophil activation test was performed using the patient

60 Allergic response was analyzed ex vivo (basophil activation test) and in vitro (RBL-2H3 mast cel

61 on the use of component-resolved approaches, basophil activation test, and novel technologies for imp

62 hil leukemia cell assay, and ex vivo using a basophil activation test, respectively.

63 Allergenicity was analyzed by basophil activation test.

64 nd its allergenic activity was analyzed in a basophil activation test.

65 und IgE were assessed using cellular assays, basophil activation testing and ELIFAB assays.

66 iate reactions has only been demonstrated by basophil activation testing, however with suboptimal sen

67 s) using finely ground tree-nut solution and basophil activation tests (BAT) were performed.

68 stigated with PHMB ImmunoCAP (n = 32) and by basophil activation tests (BAT) with CHX and ALX (n = 37

69 ane protein 1 degranulation assays and human basophil activation tests (BATs) were used to study IgE-

70 Basophil activation tests were used to investigate react

71 Blood samples were used for basophil activation tests.

72 surface receptors that modulate IgE-mediated basophil activation threshold to design promising immuno

73 th lower thresholds of reactivity had higher basophil activation to peanut in vitro.

74 Substantial suppression of basophil activation was required to maintain long-term c

75 tween IgE and FcRI, preventing mast cell and basophil activation, and blocks IgE binding to CD23 on B

76 omote IgE-facilitated allergen presentation, basophil activation, and histamine release.

77 IgE to selectively evoke human mast cell and basophil activation, and response severity was controlla

78 a costimulatory molecule during IgE-mediated basophil activation, as shown by a significant increase

79 or inhibition of IgE binding to FcepsilonRI, basophil activation, IgE production by B cells and passi

80 locked cat- and peanut-allergic IgE-mediated basophil activation, inhibited acute release of both pre

81 Peanut OIT significantly decreased basophil activation, peanut sIgE, Ara h 1, Ara h 2, and

82 antibodies and cellular responses by ELISA, basophil activation, splenocyte proliferations, and intr

83 ction molecule 1 and 2 (STIM1 and STIM2), in basophil activation.

84 e involved in the modulation of IgE-mediated basophil activation.

85 Allergenic activity was determined by basophil activation.

86 ncluding IL-5, IL-13, and IL-9 and decreased basophil activation.

87 sphatidylethanolamine, modulate IgE-mediated basophil activation.

88 d by ELISA, and IgG blocking was assessed by basophil activation.

89 B cell, platelet, neutrophil, and mast cell/basophil activity.

90 aining allergen to the percentage of CD63(+) basophils after stimulation with anti-FcepsilonRI antibo

91 ations, the AUC of dose-response curves, and basophil allergen threshold sensitivity (CD-sens) with p

92 toneal cells provided a detailed road map of basophil and mast cell development.

93 cing analyses, and cell fate assays to chart basophil and mast cell differentiation at single-cell re

94 tometry data reconstructed a detailed map of basophil and mast cell differentiation, including a bifu

95 ction and immunopathology; others, including basophil and plasmacytoid dendritic cell depletion, corr

96 A combination of baseline basophil and serologic biomarkers defined a subset of pa

97 wnregulation of SYK in both peripheral blood basophils and basophils developed from CD34(+) progenito

98 hours with anti-IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

99 y IgE receptor FcepsilonRI on mast cells and basophils and drives allergic inflammation upon secondar

100 MRGPRX2 was significantly expressed by basophils and eosinophils but not neutrophils.

101 We aimed to investigate whether human basophils and eosinophils express functional MRGPRX2.

102 c allergic inflammation to study the role of basophils and eosinophils for induction of pathology.

103 ation and signaling mechanisms of MRGPRX2 on basophils and eosinophils might enable the development o

104 erformed in highly purified peripheral blood basophils and eosinophils of atopic and nonatopic donors

105 emergence of PD-L1 checkpoint expression in basophils and eosinophils.

106 profloxacin but not PMX-53 was functional on basophils and eosinophils.

107 that recovers a key missing branchpoint into basophils and expands our understanding of the underlyin

108 de mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type

109 Basophils and IgE contribute to MCTD pathophysiology and

110 were used to investigate the contribution of basophils and IgE in the lung pathology development of t

111 We sought to investigate the role of basophils and IgE in the pathophysiology of MCTD.

112 s erythematosus and other diseases involving basophils and IgE in their pathogenesis.

113 Basophils and IgE play a role in the development of syst

114 These features included basophils and increased mast cell contents; increased im

115 ajectories from hematopoietic progenitors to basophils and mast cells are largely uncharted at the si

116 Basophils and mast cells contribute to the development o

117 Secretion from human basophils and mast cells requires spleen tyrosine kinase

118 E levels and causes FcepsilonRI receptors on basophils and mast cells to be downregulated.

119 mune cells such as macrophages, eosinophils, basophils and mast cells.

120 e the expression of CD300 receptors on human basophils and their implication in IgE-mediated basophil

121 es could modulate SYK expression in maturing basophils and whether interaction with FcgammaRIIb/CD32b

122 ly expressed on eosinophils, mast cells, and basophils and, when engaged on eosinophils, can cause ce

123 entiation into erythrocytes, megakaryocytes, basophils, and granulocytes, but not macrophages.

124 une cells, including eosinophils, mast cells/basophils, and inflammatory dendritic cells.

125 s required for IL-9 production from T cells, basophils, and mast cells in a food allergy model, and d

126 duced by many cell types, including T cells, basophils, and mast cells.

127 ress FcepsilonRIalpha, including mast cells, basophils, and plasmacytoid dendritic cells (pDCs), are

128 Basophil anergy thus seems to function as activation bar

129 n degranulation and cytokine production when basophils are activated in the presence of CD300c cross-

130 Mast cells and basophils are central to acquired resistance against blo

131 Basophils are evolutionarily conserved in vertebrates, d

132 Basophils are important effector cells involved in the p

133 Basophils are innate immune cells associated with type 2

134 Basophils are innate immune cells that support host-prot

135 Mast cells and basophils are main drivers of allergic reactions and ana

136 IgE-bearing basophils are recruited to inflamed skin via CXCL12 and

137 So far the effects of IL-31 on human basophils are unknown.

138 rtant in eosinophilic asthma and that sputum basophil assessment could be a useful additional indicat

139 After avoidance, basophil AUC rebounded in subjects with TD but not those

140 Basophil AUC rebounds after avoidance in subjects with T

141 Basophil AUC to Ara h 2 was suppressed after OIT equally

142 To analyse the functional role of IL-31 in basophil biology.

143 ctly induces activation of IL-3-primed human basophils, but IL-33 and other cytokines were dispensabl

144 rly stages with mast cells, eosinophils, and basophils, but separate from other myeloid and lymphoid

145 ne disease suggest that IVIG induces IL-4 in basophils by enhancing IL-33 in SIGN-related 1-positive

146 Mechanistically, IVIG induced IL-4 in human basophils by interacting with basophil surface-bound IgE

147 Activation of basophils by IVIG led to enhanced expression of CD69 and

148 SEEs can activate basophils by simultaneously binding as antigens in the c

149 Taken together, our results show that basophils can enhance the innate immune response to bact

150 equate for quantification of upregulation of basophil CD203c and identification of a population of CD

151 BATs to measure upregulation of basophil CD203c and induction of a CD63(hi) basophil pop

152 Milk-induced basophil CD63 expression was transiently reduced in whol

153 ts of these drugs on the growth of the human basophil cell line KU812 and the human mast cell line HM

154 Moreover, after CLP, mice whose basophils could not produce TNF, exhibited reduced neutr

155 factor CEBPA The fine-mapped variant at this basophil count association near CEBPA overlapped an enha

156 loci, including at a previously undiscovered basophil count-associated locus near the master hematopo

157 phils (P-heterogeneity < 0.001 for all), but basophil counts were similar across diet groups; in Brit

158 he urticaria activity score and with reduced basophil counts.

159 In vitro, Notch inhibition limited basophil cytokine production in response to cytokine sti

160 y cytokine that was significantly reduced in basophil-deficient mice after CLP.

161 Here we demonstrate that basophil-deficient mice exhibit reduced bacterial cleara

162 IgE activities were tested in basophil degranulation assays.

163 rified rRhi o 2 displayed IgE-reactivity and basophil degranulation with sera from all cyclophilin-po

164 IgE recognition of Cyp c 1, Cyp c 1-specific basophil degranulation, and Cyp c 1-induced allergic sym

165 -10 secretion, and inhibited Phl p 5-induced basophil degranulation.

166 s for 60min, led to an important decrease of basophil degranulation.

167 Additionally, we show that ILC2s from basophil-depleted mice express reduced amounts of the re

168 nhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to

169 Basophil depletion and IgE-deficient animals were used t

170 Basophil depletion dampened lung pathology, and IgE defi

171 reported that during pulmonary inflammation, basophil-derived interleukin-4 can act on lung-infiltrat

172 f SYK in both peripheral blood basophils and basophils developed from CD34(+) progenitors.

173 cytic subsets in the tumor microenvironment: basophils, eosinophils, and immature, intermediate, and

174 ated CRTH2 downregulation in eosinophils and basophils established a COVID-19 signature.

175 nd that mice with genetic ablation of Tnf in basophils exhibited reduced systemic concentrations of T

176 Basophils express high-affinity IgE receptors (Fcepsilon

177 We demonstrate that basophils express the activating receptor CD300c, which

178 ous urticaria and was released from isolated basophils following either anti-IgE, IL-3 or fMLP stimul

179 hetic analogs of AD-I were found to activate basophils from allergic patients.

180 rossed the Caco-2 monolayer did not activate basophils from an alpha-Gal allergic patient.

181 ignificantly increased at 08:00 vs. 20:00 in basophils from asthmatics but not controls.

182 Isolated circulating basophils from healthy donors were cultured in the prese

183 ple allergen-induced upregulation of CD63 on basophils from nontreated individuals with birch pollen-

184 gnition of these structures was evaluated in basophils from patients with selective reactions to CLV

185 Basophils from patients with systemic lupus erythematosu

186 s muris However, the mechanisms required for basophil function and gene expression regulation in this

187 t to investigate the effect of IVIG on human basophil functions.

188 dings demonstrate that Notch is required for basophil gene expression and effector function associate

189 2 immune responses involving eosinophil and basophil granulocytes, mast cells and humoral factors su

190 Additionally, PLZF-deficient basophils had reduced expression of the IL-18 receptor,

191 l importance but mast cells, antibodies, and basophils have few or no nonredundant roles.

192 Basophils have nonredundant roles in various immune resp

193 he alpha chain of FcepsilonRI, the mast cell/basophil high affinity IgE receptor.

194 using the basophil activation test (BAT) and basophil histamine release assay (BHRA).

195 to quantify absorbed Ara h 2 and 6, and the basophil histamine release assay and the human passive c

196 induce anaphylaxis and deplete mast cell and basophil IgE, but mv mAbs still strongly suppress IgE-me

197 that loss of STIM1, but not STIM2, impaired basophil IL-4 production after stimulation with immunogl

198 IL-3, loss of STIM2, but not STIM1, reduced basophil IL-4 production.

199 One of these analogs was able to activate basophils in 59% of patients whereas CLV only in 41%.

200 il progenitors in the bone marrow and mature basophils in multiple peripheral tissues.

201 ion for the variability in SYK expression in basophils in the general population.

202 emonstrate IL-9 production in mast cells and basophils in vivo requires Il9 CNS-25, and that Il9 CNS-

203 vity, the ratio of the percentage of CD63(+) basophils induced by the alpha-gal-containing allergen t

204 epsilonRI complexes activates mast cells and basophils, initiating the allergic response.

205 Mice lacking basophil-intrinsic functional Notch signaling had impair

206 Basophil-intrinsic Notch signaling was required for T. m

207 d identification of a population of CD63(hi) basophils, irrespective of whether the specimens were an

208 hanism of modulating SYK expression in human basophils is aggregation of FcepsilonRI.

209 dependent histamine release in ex vivo blood basophils is largely suppressed in a leukemia patient tr

210 Yet, how IL-9 is regulated in mast cells or basophils is not well characterized.

211 sitized mice were investigated by ELISA, rat basophil leukemia assay, T-cell proliferation experiment

212 as cell-bound IgE was measured by ELISA, rat basophil leukemia cell assay, and ex vivo using a basoph

213 NFAT-DsRed rat basophil leukemia cell attachment and retention during w

214 HBI-IgE binding, degranulation assays of rat basophil leukemia cells for in vitro efficacy, and mouse

215 as they hardly induced degranulation of rat basophil leukemia cells sensitized with Art v 1-specific

216 n in cellular degranulation assays using rat basophil leukemia cells.

217 s, is also important for the myeloid-derived basophil lineage.

218 ased intestinal type 2 inflammation, altered basophil localization in the intestine, and decreased CD

219 We show that during T. muris infection, basophils localized to the intestine and up-regulated No

220 Granulocytic (neutrophil, eosinophil, and basophil) markers were enriched during COVID-19 and disc

221 sly uncharacterized population of peritoneal basophil-mast cell progenitors.

222 Our findings suggest that basophils may be particularly important in eosinophilic

223 Platelet MPs (3.5-fold; P < .01) and basophil MPs (2.5-fold; P < .05) were increased only in

224 E receptor [FcepsilonRI](+)c-kit(+)MPs), and basophil MPs (CD203c(+)c-kit(-)MPs).

225 Reactivity of CU patients' peripheral blood basophils (n=60) to specific anti-FcepsilonRI and IgE-in

226 Sputum basophil numbers are increased in allergic asthmatics, b

227 body temperatures, plasma histamine levels, basophil numbers, antigen-specific IgE, cytokine levels,

228 nt activation and histamine release in blood basophils obtained from allergic patients (n=11) and non

229 In basophils of allergic subjects, tricolor granulocyte act

230 e alpha-Gal lipids were able to activate the basophils of an alpha-Gal allergic patient in a dose-dep

231 HLA IgE triggered mediator release in coated basophils on stimulation with specific MHC/HLA antigens.

232 This suggests that IgE-activated basophils orchestrate the recruitment of eosinophils by

233 e a peripheral basopenia and activated blood basophils overexpressing C-C chemokine receptor 3.

234 < 0.01), and blood eosinophil (P < 0.01) and basophil (P < 0.01) counts increased and plasma tryptase

235 We sought to assess the utility of different basophil parameters (basophil reactivity and sensitivity

236 Basophil phenotypes were also analyzed from IVIG-treated

237 Basophils play a pivotal role in allergic inflammation.

238 thmatics, but it is unclear what role airway basophils play in "TH2-low" asthma phenotypes.

239 on feature of type 2 inflammation, the roles basophils play in regulating these responses are unknown

240 subjects and, in particular, subjects whose basophils poorly express SYK.

241 basophil CD203c and induction of a CD63(hi) basophil population can be conducted with blood obtained

242 These studies suggest that basophils prime ILC2s to respond to neuron-derived signa

243 PLZF-deficient mice had decreased numbers of basophil progenitors in the bone marrow and mature basop

244 required for the ear swelling response, and basophils promoted the expression of eosinophil-recruiti

245 inflamed skin, IgE/FcepsilonRI-signalling in basophils promotes epithelial cell growth and differenti

246 against FceRIalpha, were linked to low blood basophil (r = .414, P = .021) and eosinophil (r = .623,

247 oxidase (IgG anti-TPO); total serum IgE; and basophil reactivity (BASO) using the basophil activation

248 he utility of different basophil parameters (basophil reactivity and sensitivity, the ratio of the pe

249 Basophil reactivity at distinct allergen concentrations,

250 with milk OIT led to distinct alterations in basophil reactivity but not T-cell responses.

251 The basophil response to anti-IgE, but not fMLP or A23187, v

252 ing the dose that induces 50% of the maximal basophil response, to Ara h 2 stimulation decreased from

253 been produced and changes in the humoral and basophil responses have been analysed.

254 Flow cytometric analysis of basophil responses implied labeling for CD63, CD203c, an

255 Basophil responses to IL-31 were assessed for chemotaxis

256 No differences in T cell or basophil responses were found between subjects on low or

257 We compared basophil responsiveness and peanut-specific immunoglobul

258 ntegrated statistical approach, we show that basophil responsiveness undergoes significant circadian

259 ly, participants entering the study with low basophil responsiveness were more likely to achieve trea

260 The altered function of basophils resulted in a blunted Th2 T cell response to a

261 responses are exaggerated in the absence of basophils, resulting in increased inflammation and dimin

262 l systems, galectin-3 is shown to facilitate basophil secretion of IL-4/IL-13, with implications that

263 ts from the production of IgE, mast cell and basophil sensitisation and degranulation, requiring a ra

264 Decrease in basophil sensitivity after three weeks of subcutaneous a

265 Decrease in basophil sensitivity after three weeks of treatment pred

266 We hypothesized that changes in basophil sensitivity and area under the curve (AUC) to t

267 immunotherapy led to a 447-fold decrease in basophil sensitivity during the first treatment year.

268 At 3 months of OIT, basophil sensitivity in subjects with SU decreased from

269 In addition, it seems that basophil sensitivity might show geographical differences

270 Early decreases in basophil sensitivity to Ara h 2 correlate with SU.

271 Total and allergen-specific IgE, IgG and basophil sensitivity were measured before and 8 weeks af

272 Basophil sensitivity, measured by using the dose that in

273 Alpha-gal-containing glycolipids activate basophils sensitized with plasma from alpha-gal allergic

274 Similarly, basophil-specific STIM1 expression was required for IgE-

275 BAT using %CD63(+) basophils (SSClow/CCR3pos) as outcome was performed with

276 4(+) T helper type 2 cells, IL-17(+) cells, basophils, substance P(+) cells, and dermal deposition o

277 Passively sensitized basophils suppressed with postavoidance SU plasma had a

278 IL-4 in human basophils by interacting with basophil surface-bound IgE but independent of FcgammaRII

279 Grass pollen-induced basophil, T-cell, and B-cell responses were evaluated be

280 The basophil-targeting effect of ibrutinib was confirmed by

281 dendritic cells and between erythrocytes and basophils that suggest multiple pathways of differentiat

282 elease was triggered in vitro by stimulating basophils that were coated with murine or human IgE-posi

283 stematically sampled the 24-hour response of basophils to IgE- and non-IgE-dependent ligands in asthm

284 ; and (3) a 10-fold increased sensitivity of basophils to profilin.

285 for T. muris-elicited changes in genome-wide basophil transcriptional programs.

286 antibodies that are bound to mast cells and basophils, triggering the release of inflammatory mediat

287 e hypothesize that ECs can directly activate basophils via cell-to-cell interaction.

288 However, a CD63(hi) population of basophils was not observed in any conditions in EDTA-tre

289 FcepsilonRI expression in basophils was required for the ear swelling response, an

290 rtions of CD63(+) and CD203c(bright)CRTH2(+) basophils were decreased following LPP treatment at V6 (

291 metric method; passive HR-IgE-stripped donor basophils were incubated with participants' serum and hi

292 Functionally, PLZF-deficient basophils were less responsive to IgE activation and pro

293 In asthmatics, basophils were positively correlated with sputum eosinop

294 obtained by means of density centrifugation, basophils were purified with a specific isolation kit, a

295 tokines, regulatory T cells, mast cells, and basophils were quantified.

296 Type 2 innate lymphoid cells and basophils were scarce in BAL fluid.

297 In contrast, when basophils were stimulated with IL-3, loss of STIM2, but

298 control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB recept

299 esults illustrate the vital role of STIM2 in basophils, which is often considered to be less importan

300 Degranulation of mast cells and basophils, with release of agents of the allergic respon