ライフサイエンスコーパス: neutrophil

1 mune complexes, compared with wild-type (WT) neutrophils.

2 nfiltration of CD4 T cells, macrophages, and neutrophils.

3 respiratory mucosa drives a robust influx of neutrophils.

4 red abundance of proinflammatory detrimental neutrophils.

5 at require enhanced or reduced production of neutrophils.

6 the regulation of bacterial phagocytosis in neutrophils.

7 ing tightly closed around the transmigrating neutrophils.

8 attack fungi that are larger than individual neutrophils.

9 the inflammatory phenotypes of LPS-activated neutrophils.

10 nse via effector cells, like macrophages and neutrophils.

11 d were linked to LTB(4) production in murine neutrophils.

12 CD11b-I weakly and is inactive toward murine neutrophils.

13 ance to CDC-induced pores on macrophages and neutrophils.

14 in primary tumors but ablates pro-metastatic neutrophils.

15 icantly decreased the frequency of ICAM-1(+) neutrophils.

16 mechanistic link to increased ROS release by neutrophils.

17 tic determinant of pustular skin disease and neutrophil abundance.

18 evidence that the alarmin S100A8/A9 mediates neutrophil accumulation during progression to chronic TB

19 ), whereas late wounds (day 7) show elevated neutrophil accumulation.

20 -/-) mice, along with reduced lesion Ly6G(+) neutrophil accumulation.

21 tic activity, pneumolysin serves as a potent neutrophil activating factor.

22 Mucosal neutrophil activation before exposure was highly predict

23 racellular ATP mitigates pneumolysin-induced neutrophil activation.

24 hat while vinculin regulates some aspects of neutrophil adhesion and spreading, it may be dispensable

25 P5K1C90 polarization, which is important for neutrophil adhesion to endothelia during inflammation.

26 ttenuates, but does not completely abrogate, neutrophil adhesion, spreading, and crawling under stati

27 oke, significantly more circulating platelet-neutrophil aggregates (PNAs) were found in CypDplt+/+ mi

28 d platelet EV generation, prevented platelet-neutrophil aggregation, and restored microvascular blood

29 tory pathways while increased eosinophils or neutrophils alone show less effect.

30 Beyond macrophages, neutrophils also accumulate in adipose and muscle tissue

31 /-) mice, which have significantly increased neutrophil and eosinophil recruitment, mucin production

32 MSU failed to trigger neutrophil and monocyte recruitment in Cd44(-/-) mice an

33 eutrophil-platelet aggregates and a distinct neutrophil and platelet activation pattern in blood, whi

34 d correlates with infiltration of monocytes, neutrophils and activated T cells.

35 A effectively blocks production of LTB(4) by neutrophils and could play a role in resolution of infla

36 Neutrophils and dendritic cells when migrating in confin

37 ion time-lapse microscopy of mouse and human neutrophils and differentiated HL-60 neutrophil-like cel

38 The presence and activation of neutrophils and eosinophils was analyzed in CRS without

39 however, significant deficits in intestinal neutrophils and eosinophils were detected in aged mice,

40 es innate immune responses by acting on both neutrophils and ILC3s through its cognate receptor free

41 animals showed a reduction in recruitment of neutrophils and macrophages in a model of sterile perito

42 eration, inflammation, steroid biosynthesis, neutrophils and macrophages infiltration, and STAT3 and

43 al differential equations, and immune cells (neutrophils and macrophages) are described individually

44 Whereas IgA2 acts pro-inflammatory on neutrophils and macrophages, IgA1 does not have pronounc

45 eficient cells is defective in chemotaxis of neutrophils and monocytes both in vitro and in vivo.

46 ardiac expression of chemokines that attract neutrophils and monocytes by 60% to 80% and lowered surf

47 The development and function of neutrophils and monocytes is primarily governed by the g

48 lonephritis to determine the contribution of neutrophils and monocytes to resolution of the condition

49 Skap2-/- neutrophils and monocytes were present in infected lungs

50 nflammatory-related white blood cell counts (neutrophils and monocytes), thereby increasing atheroscl

51 yl-peptide receptors are highly expressed on neutrophils and monocytes, and their activation promotes

52 e further demonstrate that n-apo AI binds to neutrophils and monocytes, with preferential binding to

53 ing tractions generated by both single human neutrophils and multicellular monolayers of Madin-Darby

54 ake stock of evidence for the involvement of neutrophils and NETs, to weigh the implications, and to

55 in domain-containing 3 inflammasome in naive neutrophils and promote interleukin-1beta secretion.

56 cts of the interaction between primary human neutrophils and S. aureus biofilms and provides insight

57 ce displayed increased renal infiltration of neutrophils and T cells after induction of NTS.

58 nd Cl66-Pac cells had higher infiltration of neutrophils and T helper 17 cells.

59 remarkable decrease in cardiac inflammatory neutrophils and the infiltration of inflammatory monocyt

60 mmation with infiltration of macrophages and neutrophils and upregulation of pro-inflammatory genes (

61 Patient bone marrow-derived neutrophils and white blood cells showed a severely impa

62 ent and NET formation also occurred in human neutrophils, and correlated with the incidence and sever

63 myeloid hyperplasia with predominant mature neutrophils, and decreased progenitor cells and lymphocy

64 ther chemotactic factors produced by tumors, neutrophils, and granulocytic myeloid-derived suppressor

65 dence for the systemic dissemination of rTEM neutrophils, and showed them to exhibit an activated phe

66 zebrafish model where fulvestrant inhibited neutrophil- and macrophage-dependent cancer cell dissemi

67 ster of differentiation 177 (CD177), a known neutrophil antigen, to be positively correlated with rel

68 Lung and airway neutrophils are a hallmark of severe disease in infants

69 Human neutrophils are critical for the innate immune response

70 neutrophil response to S. aureus Given that neutrophils are crucial for S. aureus clearance, underst

71 hibit disease reciprocity in which activated neutrophils are mutually shared to create collagen destr

72 Neutrophils are pivotal players in immune defence which

73 Large numbers of neutrophils are recruited into the airways of children w

74 Mechanistically, lipids stored in lung neutrophils are transported to metastatic tumor cells th

75 d autocrine/paracrine signaling required for neutrophil arrest and extravasation.

76 Here we show that pairs of neutrophils arriving closely one after another at capill

77 g, and function, plays a key role in several neutrophil-associated inflammatory disease models.

78 centrations of proinflammatory cytokines and neutrophil-attracting chemokines, and enhanced pulmonary

79 mechanism(s) driving the innate sex bias in neutrophil bactericidal capacity could identify novel ho

80 nd there was no difference in absolute blood neutrophils between groups.

81 poiesis and a more detailed understanding of neutrophil biology and function.

82 from understanding the latest discoveries in neutrophil biology and how these novel functions affect

83 Still, the role of IL-4 and IL-13 in neutrophil biology has not been well studied.

84 and provide insight into basic mechanisms of neutrophil biology.

85 uding most prominently Ly49D(+) NK cells and neutrophils, but not microglia.

86 rophil depletion nor the enhancement of lung neutrophils by administration of the chemoattractant CXC

87 isms controlling IL-1alpha/beta release from neutrophils by inhibiting caspase-8-dependent apoptosis

88 Cytokine-primed neutrophils can undergo a nonapoptotic type of cell deat

89 tment, phagocytosis and killing functions of neutrophils, causing susceptibility to pulmonary A. fumi

90 and live imaging in zebrafish revealed that neutrophil chemoattractant synthesis is triggered by a s

91 actor-alpha (TNF-alpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1).

92 eals significant reductions in expression of neutrophil chemoattractants MIP-2alpha and CXCL5 in AAA

93 d protein glycosylation (2 of 2), and normal neutrophil chemotaxis (1 of 1), and bactericidal activit

94 In addition, IL-17-induced neutrophil chemotaxis was dependent on CXCR2 signaling.

95 does simple diffusion, which may facilitate neutrophil chemotaxis.

96 Neutrophils constitute the largest population of phagocy

97 We conclude that neutrophils contribute to vascular inflammation and athe

98 g/dose, days 1-5 and day 15 through absolute neutrophil count > 500/uL]).

99 (LDH) level, ferritin level, d-dimer level, neutrophil count, and neutrophil-to-lymphocyte ratio wer

100 ve protein, white blood cell count, absolute neutrophil count, and procalcitonin (PCT), specifically

101 owed us to maintain stable circulating HoxB8 neutrophil counts for several days.

102 lso used to identify changes associated with neutrophil counts in the airway.Measurements and Main Re

103 The anti-neutrophil cytoplasmic antibody (ANCA)-associated vascul

104 ytes were present in infected lungs, and the neutrophils degranulated normally in response to K. pneu

105 creased anti-inflammatory IL-1RA and reduced neutrophil degranulation, phagocytosis, and NETosis.

106 In vivo neutrophil depletion altered the systemic and peritoneal

107 Neither neutrophil depletion nor the enhancement of lung neutrop

108 Signaling by G-CSF, a regulator of neutrophil development, trafficking, and function, plays

109 Primary neutrophil disorders typically result from disabling mut

110 Ptpn6(DeltaPMN) neutrophils displayed increased p38 mitogen-activated pr

111 Female neutrophils displayed significant up-regulation of type

112 , our data provide a time-resolved census of neutrophil diversity and gene expression dynamics in the

113 Neutrophil diversity and plasticity underlie the dual po

114 loperoxidase (MPO), a key enzyme released by neutrophils during inflammation, has been shown to catal

115 Neutropenia and neutrophil dysfunction cause serious infections and infl

116 ke S100A7, S100A12), chemotactic factors for neutrophils (e.g. CXCL5, CXCL8) and neutrophilic infiltr

117 ases characterized by the presence of excess neutrophil elastase (NE) activity in tissues, including

118 The protease neutrophil elastase (NE) has been implicated in the form

119 l breath tests to monitor dynamic changes in neutrophil elastase activity during lung infection and t

120 P96), are produced through cleavage by human neutrophil elastase and aggregate lipopolysaccharide (LP

121 ioration in airway obstruction, reduction in neutrophil elastase and inflammation.

122 spirometry decline (n = 60) and plasma anti-neutrophil elastase capacity (n = 20).Measurements and M

123 e sheep model, ewes inhaled CFTR(inh)172 and neutrophil elastase for 3 days, which resulted in prolon

124 cy of a protease inhibitor therapy targeting neutrophil elastase for the treatment of alpha-1 antitry

125 that seen in the previously determined EapH1-neutrophil elastase structure.

126 sforming growth factor beta1), downstream of neutrophil elastase, decreased mucociliary parameters in

127 eared to be mediated via their production of neutrophil elastase, was rendered less effective.

128 role is to protect lung tissue by inhibiting neutrophil elastase.

129 nfiltration (CD3 + T cells, macrophages, and neutrophils), elastic fiber disruption, and an increase

130 onal cues across venular walls, thus causing neutrophils engaged in diapedesis to reenter the systemi

131 cluster revealed that genes associated with neutrophil/eosinophil activities were up-regulated in no

132 Although neutrophils express the cytoskeletal protein vinculin, t

133 We previously showed that anti-neutrophil extracellular trap (NET) rheumatoid arthritis

134 ro, AZM198 led to a significant reduction in neutrophil extracellular trap formation, reactive oxygen

135 ils play a crucial role in sepsis, releasing neutrophil extracellular traps (NETs) composed of DNA co

136 ich foster inflammation through discharge of neutrophil extracellular traps (NETs).

137 s (MDSCs) from cancer patients extrude their neutrophil extracellular traps (NETs).

138 a process of release of histones and DNA as neutrophil extracellular traps (NETs).

139 t in the lung, kidney, and heart, containing neutrophil extracellular traps associated with platelets

140 Neutrophil extracellular traps cell death in CRSwNP was

141 ever, neutrophils were less prone to undergo neutrophil extracellular traps cell death in the tissue

142 demonstrate the importance of neutrophil extracellular traps in helminth damage after

143 of the inflamed cremaster muscle at sites of neutrophil extravasation, as visualized by fluorescent m

144 Using a new model to track neutrophil fates, we found short but variable lifetimes

145 hanistic study demonstrates that IgE induces neutrophil FcepsilonR1 expression, activates MAPK signal

146 CC involved platelets, neutrophils, fibrin, and extracellular DNA.

147 CGD neutrophils formed more numerous and larger clusters in

148 Highly purified neutrophils from healthy donors were primed in vitro wit

149 tophagy-modifying agents and azithromycin in neutrophils from healthy subjects were similar between t

150 munomodulatory properties that protect human neutrophils from injury and provides insight into its mo

151 Neutrophils from patients with acute Crohn's disease, rh

152 More important, neutrophils from septic patients showed increased ABCA1

153 ntage would be exploited by pathogens unless neutrophils from the blood stream intervened.

154 We further demonstrated improved neutrophil function: normal oxidative burst (in 3 of 3 p

155 adhesion molecules that regulate a number of neutrophil functions.

156 ome module specialized for innate immune and neutrophil functions.

157 , the lipocalin-2 (Lcn2) gene, which encodes neutrophil gelatinase-associated lipocalin (NGAL) had th

158 xpression of the MR and downstream molecules neutrophil gelatinase-associated lipocalin, galectin-3,

159 In summary, this comprehensive neutrophil granule glycome map, the first of its kind, h

160 granulopoiesis in the bone marrow, distinct neutrophil granules are successively formed.

161 isms regulating protein glycosylation during neutrophil granulopoiesis and a more detailed understand

162 echanistically, newly generated, circulating neutrophils have lower Ly6G membrane expression, and con

163 e properties, as opposed to the high-density neutrophils (HDN).

164 t insights into the mechanisms that maintain neutrophil homeostasis.

165 s) and potentially harmful (ie, reduction of neutrophils) imprints in the cellular immune system in a

166 Biodistribution of liposome-loaded neutrophils in a human-disease-relevant myocardial ische

167 ese data shed new light on the importance of neutrophils in AMI to Y. pestis and may provide a new co

168 Combined elevated sputum eosinophils+neutrophils in asthma associated with lowest lung functi

169 onocytes, natural killer cells, T cells, and neutrophils in severe COVID-19 are summarized.

170 d association of Ab-opsonized Y. pestis with neutrophils in the dermis in a mouse model of bubonic pl

171 s reconnaissance cells to recruit additional neutrophils in the event of bacterial dissemination to t

172 l a process of local tissue specification of neutrophils in the ischemic heart characterized by the a

173 The small population of neutrophils in the lymph node can act as reconnaissance

174 osis/killing by an oxidative burst of murine neutrophils in vitro Intravital microscopy (IVM) showed

175 Bacteria have evolved mechanisms to escape neutrophils, including the secretion of leucocidins (e.g

176 pregulation of cathepsin B, Tnf and Bid in a neutrophil-independent manner.

177 Mechanistically, neutrophils induce iron-dependent accumulation of lipid

178 ong inflammatory responses in the lungs with neutrophil infiltration and edema, further confirmed as

179 owed deeper bacterial penetration and denser neutrophil infiltration in the dermis.

180 rization, fibrin depositions, macrophage and neutrophil infiltration in the placenta did not differ b

181 rine model of sterile kidney injury, reduced neutrophil infiltration, and serum creatinine levels wer

182 ed increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experienci

183 erol biosynthesis, increased infiltration of neutrophils, inflammatory monocytes, and T cells, and in

184 t IL-4 receptor signaling in mouse and human neutrophils inhibited their migration toward CXCL2 and C

185 y and inflammatory disorders hinge on the EC-neutrophil interaction.

186 b had a dramatic effect in vivo on Y. pestis-neutrophil interactions in the dermis and dLN very early

187 ular permeability changes and recruitment of neutrophils into alveolar spaces, which might be linked

188 In parallel, adoptive transfer of WT neutrophils into Par4(-/-) mice restored inflammation re

189 the early epithelial transmigration of human neutrophils into the airspace in response to A. fumigatu

190 cine was independent of GEF-H1, supporting a neutrophil-intrinsic mode of action.

191 roinflammatory elastase-related proteases in neutrophils is observed in patients with CatC deficiency

192 the combined infiltration of macrophages and neutrophils is required for autoreactive CD4 T cell-medi

193 r, the mechanism(s) driving this sex bias in neutrophil killing have not been reported.

194 ical for the induction of optimal antifungal neutrophil killing of A. fumigatus spores.

195 ntracellular survival and protection against neutrophil killing.

196 The accumulation of circulating low-density neutrophils (LDN) has been described in cancer patients

197 d human neutrophils and differentiated HL-60 neutrophil-like cells (dHL-60) labeled with fluorescent

198 neutrophil subsets fit into the bone marrow neutrophil lineage remains unclear.

199 al respiratory rate, white blood cell count, neutrophil/lymphocyte ratio, and lactate dehydrogenase l

200 o identify genes differentially expressed in neutrophils, macrophages, and epithelial cells in respon

201 The impact of Q92R-Sec61alpha1 on neutrophil maturation was validated by using HL-60 cells

202 Neutrophils may contribute to the diffuse alveolar infla

203 While neutrophils mediate estrogen-induced inflammation and ad

204 reduced survival that is, at least in part, neutrophil mediated.

205 an neutrophil peptide levels, and attenuated neutrophil-mediated endothelial cell damage.

206 eloperoxidase (MPO) plays essential roles in neutrophil-mediated immunity via the generation of react

207 ression, and more importantly, inhibition of neutrophil-mediated lung metastasis via the sustained re

208 Similarly, neutrophil microvesicles increase miR-155 and enhance NF

209 (LTB4) relays chemotactic signals to direct neutrophil migration to inflamed sites through its recep

210 Finally, VR23 effectively reduces neutrophil migration, TNF-alpha secretion, and tissue in

211 s an attractive tool for characterization of neutrophil migration.

212 delayed inflammation resolution with slower neutrophil migratory speeds and retention of neutrophils

213 We show that intestinal IR induces rapid neutrophil mobilization along with a concomitant reducti

214 -specific monoclonal antibodies to eliminate neutrophils, monocytes, or both.

215 jury, we found that RvD5 did not reduce lung neutrophil myeloperoxidase levels in PLD2(-/-) mice comp

216 ngal cells were not detected, pDCs regulated neutrophil NADPH oxidase activity and conidial killing.

217 support that bone marrow-derived, presumably neutrophil, NGAL protects from ANCA-induced NCGN by down

218 , a normal differential leukocyte count (74% neutrophils [normal range, 40%-80%], 24% lymphocytes [no

219 Splenic and bone marrow neutrophils (Nphs) from BAFF-RFP mice expressed the high

220 of individual genes that result in impaired neutrophil number or function, and provide insight into

221 ruptions in this equilibrium directly impact neutrophil numbers in circulation, cell trafficking, ant

222 Decreased neutrophil numbers in the spleen were observed during ac

223 er, T-bet(-/-) mice have augmented IL-17 and neutrophil numbers, and neutralizing IL-17 reduces the n

224 Depletion of neutrophils or S100A8/A9 deficiency resulted in improved

225 xygen species production, and released human neutrophil peptide levels, and attenuated neutrophil-med

226 compared to females, with a higher influx of neutrophils per villus at 45I-30R (4.9 [3.1-12.0] vs 3.3

227 nd both catecholamines promoted monocyte and neutrophil phagocytosis.

228 erefore, Raman spectroscopy enables reliable neutrophil phenotyping and infection diagnosis in a labe

229 Patients with COVID-19 also present with neutrophil-platelet aggregates and a distinct neutrophil

230 Neutrophils play a crucial role in sepsis, releasing neu

231 ents leads to the pulmonary sequestration of neutrophils (PMNs), which serves as the first event in t

232 ypic characterization revealed heterogeneous neutrophil populations containing Nalpha and Nbeta subty

233 In this study, we found that CGD (CYBB-) neutrophils produced higher amounts of leukotriene B4 (L

234 nulocyte colony-stimulating factor increases neutrophil production and reduces infection risk.

235 by the development of autoantibodies to the neutrophil proteins leukocyte proteinase 3 (PR3-ANCA) or

236 amples obtained biweekly from baseline until neutrophil recovery following induction chemotherapy (IC

237 decrease in circulating CXCL1, an important neutrophil recruiter and activator.

238 A key driver of neutrophil recruitment and activation is the complement

239 nds reduces neutrophil velocity and inhibits neutrophil recruitment in response to inflammation in a

240 Neutrophil recruitment in the lung of superinfected mice

241 be dispensable for beta2 integrin-dependent neutrophil recruitment in vivo.

242 Neutrophil recruitment is delayed in early wounds (12 ho

243 destly impaired CXC chemokine expression and neutrophil recruitment to the infected tongue but not to

244 ncy significantly heightened macrophages and neutrophils recruitment to the site of inflammation.

245 proteins that protect K. pneumoniae against neutrophil-related effector functions.

246 ubating linezolid (0.4-40 mg/L) with healthy neutrophils relative to those with C5a-induced injury.

247 es tissues from COVID-19 patients, and their neutrophils released higher levels of NETs.

248 potentially exhausted T cells and activated neutrophils, respectively; (2) in contrast, sCD14 and sC

249 ogether, inhibition of these two arms of the neutrophil response likely contributes to the noninflamm

250 ovides insight into how S. aureus evades the neutrophil response to cause persistent infections.

251 We aimed to investigate the role of ATP in neutrophil response to pneumococcal infections.

252 f CR3, C3, and ROS to innate sex bias in the neutrophil response to S. aureus Given that neutrophils

253 ucociliary barrier function and early airway neutrophil responses are critical for clearing fungal co

254 which might directly or indirectly influence neutrophil responses to LPS.

255 kines, chemokines, and cancer cell-recruited neutrophils result in enhanced metastasis and chemothera

256 ETs were found in the airway compartment and neutrophil-rich inflammatory areas of the interstitium,

257 an enzyme responsible for the activation of neutrophil serine proteases.

258 Collectively, our work reveals that neutrophils serve as an energy reservoir to fuel breast

259 Notably, we also found that neutrophils shed extracellular vesicles in the vascular

260 We also observed that p101(VVKR777AAAA) neutrophils showed enhanced p84-dependent ROS responses

261 n macrophages that mediate the attraction of neutrophils, shown previously to allow transfer of nucle

262 Importantly, either systemic or neutrophil-specific Akt1 deletion is sufficient to inhib

263 Herein, neutrophil subcellular granules were fractionated by Per

264 The three mature peripheral blood neutrophil subsets arise from distinct maturing bone mar

265 Still, how newly identified neutrophil subsets fit into the bone marrow neutrophil l

266 ets arise from distinct maturing bone marrow neutrophil subsets.

267 led more effectively in azithromycin-treated neutrophils, suggesting that pathogen-specific factors m

268 This can be explained by the low neutrophil surface expression of the IL-4 receptor alpha

269 hanism and possible evolutionary benefits of neutrophil swarms are elusive.

270 ed inflammation, and infection controlled by neutrophils, T(H)17 cells, B cells, and antigen-presenti

271 ur findings unveil a 'disarming' strategy of neutrophils that depletes protein stores to reduce the m

272 Strikingly, many neutrophils that migrated between EC junctions were able

273 subset, with characteristics of an immature neutrophil, that had neuroprotective properties and drov

274 High neutrophil to lymphocyte ratio (NLR) and monocyte to lym

275 fied Glasgow prognostic score (mGPS) and the neutrophil to lymphocyte ratio (NLR) and survival in pat

276 . injection confirms the ability of injected neutrophils to carry loaded liposomes to inflammation si

277 In addition, the derived neutrophil-to-lymphocyte ratio and platelet count were s

278 level, d-dimer level, neutrophil count, and neutrophil-to-lymphocyte ratio were all predictive of mo

279 ith type 2 innate lymphoid cells, monocytes, neutrophil trafficking, and T effector cells.

280 decreased smooth muscle cell activation and neutrophil transendothelial migration during AAA formati

281 At steady state, neutrophil turnover and replenishment are continually ma

282 IP5K1C90, and PM PtdIns4P in mouse and human neutrophils upon integrin stimulation.

283 l amplified the epithelial transmigration of neutrophils, using primary human airway epithelium.

284 Furthermore, one of these compounds reduces neutrophil velocity and inhibits neutrophil recruitment

285 ying FcgammaRIIIb derived from healthy donor neutrophils, we observed profound differences as compare

286 In vivo-differentiated HoxB8 neutrophils were able to migrate to the inflamed periton

287 Finally, SiglecF(hi) neutrophils were also found in atherosclerotic vessels,

288 ATC CM-primed neutrophils were cocultured with ATC cells to determine

289 In vitro, BLT1(-/-) neutrophils were defective in their ability to undergo a

290 am1 and Tnf) and Siglecf(low) (Slpi, Ifitm1) neutrophils were found.

291 ciated with bacterial colonization, however, neutrophils were less prone to undergo neutrophil extrac

292 of the interstitium, while NET-prone primed neutrophils were present in arteriolar microthrombi.

293 ction chemokine-driven airway recruitment of neutrophils, which caused enhanced disease mediated by p

294 ivator of circulating immune cells including neutrophils, which foster inflammation through discharge

295 Expression of CD71 marks proliferating neutrophils, which were expanded in the blood of melanom

296 ase COVID-19 convalescent patients had fewer neutrophils, while their cytotoxic CD8(+) T cells were a

297 Treatment of control neutrophils with COVID-19 platelet-rich plasma generated

298 neutrophil migratory speeds and retention of neutrophils within the tissues.

299 nary disease, yet the mechanisms that retain neutrophils within tissues remain poorly understood.

300 of M. abscessus However, in cystic fibrosis neutrophils, wortmannin inhibited killing of a rough cli