ライフサイエンスコーパス: eosinophil

1 tandard procedure for the isolation of human eosinophils.

2 ion in COPD should consider assessing sputum eosinophils.

3 ytes, neutrophils, natural killer cells, and eosinophils.

4 OPD severity or exacerbations, or for sputum eosinophils.

5 ules involved in Siglec-8 function for human eosinophils.

6 ophagocytosis, and an inconstant presence of eosinophils.

7 reased IL-5 and eotaxin receptors than blood eosinophils.

8 face receptor selectively expressed on human eosinophils.

9 , serum IgE, periostin, and blood and sputum eosinophils.

10 -infected mice that phenotypically resembles eosinophils.

11 n about the consequences of this stimulus on eosinophils.

12 s of allergen-induced circulating and airway eosinophils.

13 opsies, mCD48 was expressed predominantly by eosinophils.

14 r blood eosinophils are predictive of sputum eosinophils.

15 eins involved in Siglec-8 function for human eosinophils.

16 We used a sputum eosinophil 2% cut point to define subjects with either a

17 3.0 x 10(4)/mL [P < .01] and 6.9% [P < .01]; eosinophils, 2.0 x 10(4)/mL [P < .01] and 1.2% [P < .01]

18 m neutrophil (30.5 x 10(4)/mL and 23.1%) and eosinophil (7.0 x 10(4)/mL and 3.8%) numbers and percent

19 l numbers but had a limited effect on airway eosinophil activation markers, suggesting that these cel

20 sCD48 effect on CD244-dependent eosinophil activation was evaluated.

21 Serum interleukin 5 levels and eosinophil activation, as assessed by surface expression

22 sCD48 inhibited anti-CD244-induced eosinophil activation.

23 -dependent asthmatic patients with increased eosinophil activity, recurrent pulmonary infections, or

24 Blood eosinophils adhering to adsorbed periostin were imaged a

25 IL-5 enhances eosinophil adhesion and migration on periostin, an extra

26 After eosinophil adhesion, we observed reactive oxygen species

27 ment promotes rapid beta2-integrin-dependent eosinophil adhesion.

28 Blood eosinophils alone were not a reliable biomarker for COPD

29 Despite differences in eosinophil and lymphocyte counts during the first 24 hou

30 For instance, both eosinophil and neutrophil counts are often increased in

31 Moreover, nebulization of NSC23766 decreased eosinophil and neutrophil populations in bronchoalveolar

32 challenge phase led to a marked reduction of eosinophil and T cell numbers in bronchoalveolar lavage

33 ed production of IL-5, prostaglandin D2, and eosinophil and T-helper type 2 cell chemokines compared

34 has significantly added to our knowledge of eosinophils and eosinophil-associated diseases.

35 hed the allergen-induced rise in circulating eosinophils and expression of IL-3 receptors, whereas ai

36 ch are characterized by type 2 inflammation, eosinophils and group 2 innate lymphoid cells (ILC2s).

37 patients showed the highest levels of sputum eosinophils and had a high body mass index.

38 Finally, CysLT1R(-/-) mice had reduced lung eosinophils and ILC2 responses after exposure to the fun

39 ntary effects and suppressed BALF and tissue eosinophils and inflammation, MSC numbers, reduced the p

40 severity of acute AAD by suppressing tissue eosinophils and inflammation, mucus-secreting cell (MSC)

41 lectin-10-containing immune synapses between eosinophils and lymphocytes.

42 ) mice displayed age-related accumulation of eosinophils and macrophages in the adipose tissue and de

43 ine whether Siglec-8 is endocytosed in human eosinophils and malignant mast cells, identify mechanism

44 CD48 is a membrane receptor (mCD48) on eosinophils and mast cells and exists in a soluble form

45 henotypes with enhanced skin infiltration of eosinophils and mast cells, elevation of T helper type 2

46 infiltration of colon and lung parenchyma by eosinophils and mast cells.

47 d in decreased C5aR2 expression in pulmonary eosinophils and monocyte-derived dendritic cells.

48 mmatory features of asthma, including sputum eosinophils and mucins, as well as acute airway response

49 maT notably reduced pre-LPS challenge sputum eosinophils and mucins, including mucin 5AC and reduced

50 -5, and IL-13, resulting in increased airway eosinophils and mucus hypersecretion.

51 nd significantly reduced the total number of eosinophils and neutrophils 48 hour and 96 hour after th

52 This study included the activation state of eosinophils and neutrophils in peripheral blood to pheno

53 Eosinophils and neutrophils in the submucosa were quanti

54 ked by an influx of neutrophils (mainly) and eosinophils and secretion of IL-6, TNF-alpha, and IL-17

55 tdTomato-C3aR(+) Interestingly, most tissue eosinophils and some macrophage populations expressed C3

56 consistently caused extensive cell death in eosinophils and the human mast cell leukemia cell line H

57 Eosinophils and their associated cytokines IL-4 and IL-5

58 per airway symptoms, an enrichment of ILC2s, eosinophils, and neutrophils, along with increased produ

59 aeroallergen sensitization, peripheral blood eosinophils, and serum periostin as potential biomarkers

60 Siglec-8 mAb or glycan ligand binding causes eosinophil apoptosis associated with reactive oxygen spe

61 nases completely prevented Siglec-8-mediated eosinophil apoptosis.

62 itor) completely inhibited Siglec-8-mediated eosinophil apoptosis.

63 osteroids (GCS), agents that normally induce eosinophil apoptosis.

64 Eosinophils are a subset of granulocytes that can be inv

65 Eosinophils are immunomodulatory leucocytes that contrib

66 Eosinophils are likely to be specifically recruited to S

67 Eosinophils are multifunctional cells of the innate immu

68 Eosinophils are phenotypically and functionally heteroge

69 er exacerbation frequency, and whether blood eosinophils are predictive of sputum eosinophils.

70 n eosinophil-deficient mice, confirming that eosinophils are required for IgE-mediated tissue injury.

71 enoceptors by catecholamines, and identified eosinophils as a novel source of these mediators.

72 Group 1 had the highest submucosal eosinophils, as well as high fractional exhaled nitric o

73 ly added to our knowledge of eosinophils and eosinophil-associated diseases.

74 counts (neutrophils, monocytes, lymphocytes, eosinophils, basophils) differ by ethnicity.

75 In PR-GOAL WBC types (ie, neutrophils, eosinophils, basophils, lymphocytes, and monocytes) in p

76 es relevant to basic and clinical aspects of eosinophil biology, a search of articles published since

77 effects of hypoxia on several key aspects of eosinophil biology, namely secretion, survival, and thei

78 ut mepolizumab induced a rise in circulating eosinophils, bronchoalveolar lavage eosinophilia, and eo

79 m periodontitis patients are able to produce Eosinophil Cationic protein and histamine in response to

80 y found that neutrophils produce and release Eosinophil Cationic Protein and histamine, two important

81 cale epidemiological approach, we identified eosinophil cationic protein as an independent and predic

82 However, neutrophil-derived histamine and Eosinophil Cationin Protein production and their role ha

83 en induced markedly reduced levels of airway eosinophils, CD4(+) lymphocyte infiltration, and mucus p

84 otypes were defined by sputum neutrophil and eosinophil cell proportions.

85 ed patients on the basis of blood and sputum eosinophil concentrations and compared their demographic

86 We aimed to assess whether high eosinophil concentrations in either sputum or blood are

87 We also analysed whether blood eosinophil concentrations reliably predicted sputum eosi

88 hil concentrations reliably predicted sputum eosinophil concentrations.

89 However, new information suggests that eosinophils contribute more broadly to inflammatory resp

90 Concurrent experiments showed that eosinophils contributed to intravascular thrombosis by e

91 Using either a PC20 </=16 mg/mL or a sputum eosinophil count >/=1% increased the sensitivity to 94%.

92 A FeNO level >/=25 ppb and a sputum eosinophil count >/=2% provided lower sensitivity rates

93 NSBH despite a positive SIC showed a sputum eosinophil count >/=2%, a FeNO level >/=25 ppb, or both

94 phenotype were stratified according to blood eosinophil count (>/=150 per cubic millimeter at screeni

95 >/=3%, and <5% and >/=5%) and absolute blood eosinophil count (<150 cells/mul, 150 to <300 cells/mul,

96 mly allocated them (1:1; stratified by blood eosinophil count [<300 cells per muL vs >/=300 cells per

97 most well established of these are the blood eosinophil count and serum periostin, both of which have

98 tment reduces STH prevalence, total IgE, and eosinophil count but has no effect on IR at the communit

99 treatment for COPD have shown that the blood eosinophil count is associated with the risk of COPD exa

100 l due to clinical relevance]), rectal biopsy eosinophil count less than or equal to 32 cells per high

101 Eosinophil count of 300 cells/muL or more and aeroallerg

102 In METREO, all patients had a blood eosinophil count of at least 150 per cubic millimeter at

103 EC) in the first 24 hours posttreatment, the eosinophil count rose significantly in both groups, peak

104 The mean blood eosinophil count was 200/muL (SD, 144/muL).

105 The combination of blood eosinophil count, fractional exhaled nitric oxide, Asthm

106 to an increased body mass index or a reduced eosinophil count.

107 revalence, total immunoglobulin E (IgE), and eosinophil count.

108 ed nitric oxide values (14.5 ppb), and blood eosinophil counts (96 cells/muL) than all other groups.

109 weak but significant association with sputum eosinophil counts (receiver operating characteristic are

110 ifferentials, explaining 71% of variation in eosinophil counts and 64% of variation in neutrophil cou

111 T-cell counts and positively correlated with eosinophil counts and not associated with CD4 T-cell cou

112 values of NSBH, and FeNO, as well as sputum eosinophil counts assessed at baseline of the SIC were d

113 s was found among patients with higher blood eosinophil counts at screening.

114 AER among patients with baseline blood eosinophil counts of at least 0 cells per muL was 1.16 (

115 Blood eosinophil counts showed a weak but significant associat

116 DSQ scores were 29.3 and 29.0, and mean peak eosinophil counts were 156 and 130 per hpf in the BOS an

117 DSQ scores were 15.0 and 21.5, and mean peak eosinophil counts were 39 and 113 per high-power field,

118 inophil counts, rather than sputum or tissue eosinophil counts, evolved as a pharmacodynamic and pred

119 and allergic mediators, lower mast cells and eosinophil counts, lower protein expressions of Th2 cyto

120 inical development program showed that blood eosinophil counts, rather than sputum or tissue eosinoph

121 cantly predicted the presence of high sputum eosinophil counts.

122 eived placebo, independent of baseline blood eosinophil counts.

123 ively, active vs placebo) and gastric mucosa eosinophils counts (239 eosinophils/mm(2) [59-645] vs 25

124 CSF) was detected in supernatants of ex vivo eosinophil cultures from the lungs of fungal allergen-ch

125 We report that adhesion-induced eosinophil cytolysis takes place through RIPK3-MLKL-depe

126 imed to elucidate the molecular mechanism of eosinophil cytolysis.

127 g Chlamydia infection), whereas studies with eosinophil-deficient mice identified this innate immune

128 ore, IgE autoantibodies fail to induce BP in eosinophil-deficient mice, confirming that eosinophils a

129 ability of sputum immunoglobulins to induce eosinophil degranulation in vitro was assessed.

130 with increased autoantibody levels triggered eosinophil degranulation in vitro, with release of exten

131 impact of activation with IL-3 on IgG-driven eosinophil degranulation.

132 ermal-epidermal separation by IL-5-activated eosinophils depends on adhesion and Fcgamma receptor act

133 l (CLC) formation, which was most evident in eosinophils derived from atopic and asthmatic donors; (i

134 results provide evidence that IL-5-activated eosinophils directly contribute to BP blister formation

135 Eosinophils drove progression to DCMi through their prod

136 ha was predominantly expressed on esophageal eosinophils during EoE, in addition to select cells with

137 study, we demonstrate an unexpected role of eosinophils during plasmatic coagulation, hemostasis, an

138 A CD16(hi) subset of eosinophils, encompassing 1-5% of all eosinophils, was a

139 However, steroid-insensitive patients with eosinophil-enriched inflammation have also been describe

140 About 8.8% +/- 4.8% of the infiltrating eosinophils exhibited EETs in patients' nasal polyp tiss

141 Leukotriene C4 synthase-deficient eosinophils exhibited impaired chemotaxis to CCL19 that

142 Whether DNA methylation of eosinophils explains these findings is insufficiently un

143 onclude, we describe a subset of suppressive eosinophils expressing CD16 that may escape detection be

144 f prolonged survival ex vivo, in contrast to eosinophils from both untreated and fungal allergen-chal

145 Blood eosinophils from children and adults with EoE, and healt

146 Eosinophils from children with EoE also had higher level

147 A smaller fraction of eosinophils from children with EoE expressed CD44 and a

148 As shown here, eosinophils from fungal allergen-challenged wild-type mi

149 his response in a disease model, we isolated eosinophils from the livers of Schistosoma mansoni-infec

150 Furthermore, eosinophils from the lungs and spleen of fungal allergen

151 The transfer of eosinophils from the lungs of allergen-sensitized and ch

152 Eosinophils from the spleens of IL-5 transgenic mice, fl

153 After 2 d of coculture, 11% of the eosinophils gained CD16 expression.

154 p versus controls, while Th1, Th2, Treg, and eosinophil gene signatures were increased in patients wi

155 Additionally, the eosinophil granule proteins major basic protein and eosi

156 rface expression of CD69 and serum levels of eosinophil granule proteins, were increased posttreatmen

157 intact granules, so-called clusters of free eosinophil granules.

158 EV1 percentage predicted than the low sputum eosinophil group both before (65.7% [IQR 51.8-81.3] vs 7

159 The high sputum eosinophil group had significantly lower median FEV1 per

160 The high blood eosinophil group had slightly increased airway wall thic

161 were significantly higher in the high sputum eosinophil group than the low sputum eosinophil group.

162 sputum eosinophil group than the low sputum eosinophil group.

163 icantly different between low and high blood eosinophil groups, but differences were less than those

164 epolizumab treatment, bronchoalveolar lavage eosinophils had more surface IL-3 and granulocyte-monocy

165 Eosinophils have been found in the airways, tissues, and

166 IONALE: Post hoc analyses suggest that blood eosinophils have potential as a predictive biomarker of

167 Eosinophils have the capacity to regulate the function o

168 ined by symptom improvement and less than 15 eosinophils/high-power field.

169 eptor significantly decreased the numbers of eosinophils, IL-13(+) type 2 innate lymphoid cells and I

170 mice restored effects of OVA on lymphocytes, eosinophils, IL-13, IL-5, and mucous hypersecretion to w

171 dy describes a large animal model of gastric eosinophil in peanut-sensitized piglets.

172 most common endpoint is a reduced number of eosinophils in biopsies, changes in symptoms and endosco

173 Increased concentrations of eosinophils in blood and sputum in chronic obstructive p

174 r 12 weeks exhibit AHR, increased numbers of eosinophils in bronchoalveolar lavage (BAL) and increase

175 s in regulating the pulmonary trafficking of eosinophils in experimental allergic asthma.

176 We investigated the role of eosinophils in mediating normal PVAT function.

177 arditis (EAM) model to determine the role of eosinophils in myocarditis and DCMi.

178 The persistence of eosinophils in sputum despite high doses of corticostero

179 l as the release of eosinophil peroxidase by eosinophils in the bronchial mucosa, was maintained afte

180 severe hepatitis and reduced accumulation of eosinophils in the liver, whereas adoptive transfer of h

181 wild-type mice, with increased retention of eosinophils in the lungs of leukotriene C4 synthase-defi

182 To investigate the role of eosinophils in the pathogenesis of BP with a specific fo

183 Virus- or viral peptide-exposed eosinophils induced CD8(+) T cell proliferation, activat

184 -5 and in the presence of BP autoantibodies, eosinophils induced separation along the dermal-epiderma

185 dependent and correlates with the degree of eosinophil infiltration in the skin.

186 induced the release of IL-33 and subsequent eosinophil infiltration into the lungs.

187 rtantly, adoptive transfer of ILC2s restored eosinophil influx and IL-4, IL-5 and IL-13 production in

188 The migration of intratracheally injected eosinophils into paratracheal lymph nodes from distal al

189 5, IL-13, eotaxin and MCP-3; infiltration of eosinophils into the airway submucosa; proliferation of

190 ain a distinct cytokine profile, and, unlike eosinophils isolated from IL5tg mice, they survive ex vi

191 Eosinophils isolated from the lungs A. alternata-challen

192 ce revealed marked and distinct increases in eosinophil levels and their production of IL-4 in the wh

193 atients with allergic asthma, baseline blood eosinophil levels and/or clinical markers of asthma seve

194 actin formation; (iv) marked prolongation of eosinophil lifespan (via a NF-kappaB and Class I PI3-kin

195 to demonstrate a primary abnormality in the eosinophil lineage.

196 , and a selective decrease in blood and BALF eosinophils, lung Il13 levels, collagen, and smooth musc

197 10), and did not colocalize with markers for eosinophils, macrophages, T cells, or B cells (n = 3-5).

198 cytoplasmic granules and express CD11b, the eosinophil marker Syglec-F, variable levels of CCR3, and

199 production, and inhibition of responses from eosinophils, mast cells, and basophils in the affected t

200 rface protein expressed selectively on human eosinophils, mast cells, and basophils, making it an ide

201 acterized by inflammatory pathways involving eosinophils, mast cells, and group 3 innate lymphoid cel

202 has defined a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-1

203 nse was independent of effects on esophageal eosinophil maturation or activation.

204 Thus, targeting eosinophils may be a promising therapeutic approach for

205 Eosinophil mCD48 expression was significantly elevated i

206 ntegrin metalloproteinase 8 (ADAM8), a major eosinophil metalloproteinase previously implicated in as

207 tion study adjusted for WBC types (including eosinophils), methylation changes in genes enriched in p

208 inhibiting neutrophil trafficking, targeting eosinophil migration and survival, and suppressing mast

209 s are involved in regulating airway and lung eosinophil migration into paratracheal lymph nodes ident

210 unts (239 eosinophils/mm(2) [59-645] vs 2554 eosinophils/mm(2) [462-8057], P < .01, respectively acti

211 ) and gastric mucosa eosinophils counts (239 eosinophils/mm(2) [59-645] vs 2554 eosinophils/mm(2) [46

212 An eosinophil molecular pattern capable of distinguishing c

213 is study were to determine whether the blood eosinophil molecular pattern of children with EoE is (i)

214 Age-related physiologic differences in eosinophil molecular patterns may partly explain the dif

215 in(+)MPs), platelet MPs (CD31(+)CD41(+)MPs), eosinophil MPs (EGF-like module-containing mucin-like ho

216 200 mg of gammaT daily for 14 days on sputum eosinophils, mucins, and cytokines.

217 wn immune cells, including T cells, B cells, eosinophils, neutrophils, dendritic cells, and NK cells.

218 subsequently followed by enhanced numbers of eosinophils, neutrophils, dendritic, and T cells into th

219 n immediate response with rapid reduction of eosinophils, normalization of liver enzymes, and amelior

220 group, younger age at recruitment, increased eosinophil number, recent exacerbation, and higher treat

221 Mepolizumab reduced airway eosinophil numbers but had a limited effect on airway eo

222 Furthermore, eosinophil numbers decreased in blood concurrently with

223 olves to foster migration of IL-5-stimulated eosinophils on a surface coated with periostin.

224 ure to IL-3 further induced degranulation of eosinophils on aggregated IgG via increased production a

225 by fluorescent microscopy, and migration of eosinophils on periostin was assayed.

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

227 iety of lymphocytes are capable of directing eosinophils or neutrophils to the lungs, but the contrib

228 s lung allergic inflammation (number of lung eosinophils, P < .005).

229 mpared treatment efficacy according to blood eosinophil percentage (<2% and >/=2%, <3% and >/=3%, and

230 recruitment, higher total IgE, higher blood eosinophil percentage and number, and higher treatment s

231 l surface markers, as well as the release of eosinophil peroxidase by eosinophils in the bronchial mu

232 ls, bronchoalveolar lavage eosinophilia, and eosinophil peroxidase deposition in bronchial mucosa.

233 3 receptors, whereas airway eosinophilia and eosinophil peroxidase deposition were blunted but not el

234 hil granule proteins major basic protein and eosinophil peroxidase were more frequently detected in t

235 terns may partly explain the different blood eosinophil phenotypes in children vs adults with EoE.

236 We conclude that adipose tissue eosinophils play a key role in the regulation of normal

237 Most macrophage and eosinophil populations were tdTomato-C3aR(+) Interesting

238 oms related to esophageal dysfunction and an eosinophil-predominant inflammation.

239 disease of the esophagus characterized by an eosinophil-predominant inflammatory infiltrate.

240 Our data suggest that eosinophils promote host cellular immunity to reduce inf

241 Sputum neutrophil proportions, but not eosinophil proportions, correlated significantly with th

242 Thus, eosinophils provide the cellular link between IgE autoan

243 phils were positively correlated with sputum eosinophils (r=0.54; P<0.005) and inversely with sputum

244 Eosinophil receptors for IL-5 share a common ss-chain wi

245 erized by ILC2 activation, proliferation and eosinophil recruitment that was associated with accelera

246 L11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airwa

247 ILC2 activation and eosinophil recruitment, TH2-related cytokine and chemoki

248 antibody that directly and rapidly depletes eosinophils, reduces asthma exacerbations, and improves

249 We propose, therefore, that eosinophils remodel and migrate on periostin-rich extrac

250 cal TNF-alpha levels, might lead to impaired eosinophil resolution and could contribute to the eosino

251 mphocyte subsets dominated the neutrophil or eosinophil response.

252 olyposis, aspirin sensitivity and neutrophil/eosinophil responsiveness upon stimulation with formyl-m

253 nally, engagement of Siglec-8 on IL-5-primed eosinophils resulted in increased phosphorylation of Akt

254 Sialidase treatment of eosinophils revealed that Siglec-8 is partially masked b

255 rs, but the ability of Siglec-8 to stimulate eosinophil ROS production and apoptosis suggests that Si

256 of lamina propria TH2 cells, mast cells, and eosinophils, shock (hypothermia), mast cell degranulatio

257 ected from DCMi like DeltadblGATA1 mice, and eosinophil-specific IL-4 deletion resulted in improved h

258 Together, our studies reveal IL-4-producing eosinophils stimulate ESC proliferation and prevent Chla

259 e disease-relevant consequences of prolonged eosinophil stimulation with IL-3.

260 henotype indicated by bronchoalveolar lavage eosinophil surface markers, as well as the release of eo

261 tor (GM-CSF; an agonist cytokine linked with eosinophil survival and activation) would be protective

262 ralizing antibodies had any impact sustained eosinophil survival ex vivo.

263 Conversely, eosinophils, Th2 T cells, type 2 innate lymphoid cells,

264 ll infiltration and a marked accumulation of eosinophils that was required for tissue protection.

265 ed with clinical judgement, a baseline blood eosinophil threshold of 150 cells/muL or greater or a hi

266 0 cells/muL or greater or a historical blood eosinophil threshold of 300 cells/muL or greater will al

267 or patients with a combination of high blood eosinophil thresholds and a history of more frequent exa

268 b for patients with different baseline blood eosinophil thresholds and exacerbation histories.

269 ely as an activating receptor on IL-5-primed eosinophils through a novel pathway involving regulation

270 biomarker than high concentrations of blood eosinophils to identify a patient subgroup with more sev

271 ding the assessment of FeNO level and sputum eosinophils to NSBH improves the identification of subje

272 IL-5 causes suspended eosinophils to polarize with filamentous (F)-actin and g

273 gently needed to explore the contribution of eosinophils to the mechanism of disease in COPD and to i

274 previously demonstrated in mice that airway eosinophils traffic from the airway lumen into lung-drai

275 roles of cysteinyl leukotrienes in mediating eosinophil trafficking from lungs to paratracheal lymph

276 However, mechanisms whereby eosinophils traverse from the lungs and home to paratrac

277 As eosinophils typically accumulate at sites that are relat

278 acuolization, and cytolysis were observed in eosinophils under in vivo inflammatory conditions.

279 that an early innate response that involves eosinophils underlies the exacerbation.

280 ociated with increased sputum neutrophil and eosinophil values and cytokine levels related to neutrop

281 inflammatory interactions of mast cells with eosinophils via its ligand CD244.

282 a currently in development focus on limiting eosinophil viability via strategic cytokine blockade, th

283 set of eosinophils, encompassing 1-5% of all eosinophils, was also identified in the blood of healthy

284 COPD severity, high concentrations of sputum eosinophils were a better biomarker than high concentrat

285 Eosinophils were also isolated from lungs of mice sensit

286 IL-17A, IL-8, IL-6, neutrophils and eosinophils were detected and quantified by immunohistoc

287 lomas were observed and only single lesional eosinophils were detected, GPTD does not resemble a gran

288 Eosinophils were dispensable for myocarditis induction b

289 Recruited eosinophils were enumerated in bronchoalveolar lavage fl

290 Eosinophils were examined in blood, bronchoalveolar lava

291 Eosinophils were identified by microscopy and flow cytom

292 Isolated blood eosinophils were incubated on glass coverslips coated wi

293 Human eosinophils were incubated with T cells that were stimul

294 10 minutes in the presence of IL-5, adherent eosinophils were polarized with PSGL-1 at the nucleopod

295 h IL-4-IRES-eGFP (4get) reporter mice showed eosinophils were the main IL-4-producing endometrial leu

296 Our experiments showed eosinophils were the major IL-4-expressing cell type in

297 Human blood eosinophils were used to establish the impact of activat

298 eage kinase-like (MLKL) signaling pathway in eosinophils, which, after its activation, leads to the p

299 ) oxidase activation because pretreatment of eosinophils with catalase (an extracellular superoxide s

300 cubated with purified human peripheral blood eosinophils with or without activation in the presence o