ライフサイエンスコーパス: PMN

1 PMN interaction with ECs induced the entry of Ca(2+) in

2 PMN migration to sites of infection/inflammation require

3 PMN were shown to generate C1q and C3a; exposure of hNSC

4 PMN-MP/MPO-dependent inhibition of IEC wound healing was

5 PMN-targeted stimulation significantly increased connect

6 PMNs isolated from gp91phox(-/-) mice significantly redu

7 The NK cell-to-Lox-1(+) PMN-MDSC ratio (NMR) was significantly higher in respond

8 y inversely correlated with that of Lox-1(+) PMN-MDSCs after the first treatment cycle.

9 ved suppressor cells (M-MDSCs), and Lox-1(+) PMN-MDSCs in peripheral blood samples of 62 NSCLC patien

10 and pro-Mmp-9 to the surface of Timp-1(-/-) PMNs.

11 n in non-responders, while the median Lox-1+ PMN-MDSC percentage showed the opposite trend.

12 igher quality, <10 SECs per LPF (but not >25 PMNs per LPF) was the microscopic variable most associat

13 low-power field (LPF) and 2350 (62%) had >25 PMNs per LPF, measures traditionally associated with spe

14 b(Mg(1/3)Nb(2/3))O(3)](0.7)-[PbTiO(3)](0.3) (PMN-PT) unclamped piezoelectric membranes with ferromagn

15 relaxor ferroelectric PbMg(1/3)Nb(2/3)O(3) (PMN).

16 hombohedral Pb(Mg(1/3)Nb(2/3))O(3)-PbTiO(3) (PMN-PT) crystals to simultaneously generate near-perfect

17 aT(c) > 30 K) in a voltage-actuated V(2)O(3)/PMN-PT [Pb(Mg,Nb)O(3)-PbTiO(3)] heterostructure.

18 plus symptoms or discharge; controls had <5 PMNs, no symptoms, no discharge.

19 onuclear leukocytes (PMNs), with up to 10(5) PMNs in clear diluted buffer from 50 muL of airway secre

20 te cellular migration, and can function as a PMN chemoattractant.

21 inate receptor (SUCNR1) inhibition abrogated PMN priming, PMN sequestration, and ARDS.

22 ibe a novel pathogenic entity, the activated PMN (polymorphonuclear leukocyte, i.e., neutrophil)-deri

23 In summary, Mtb LAM activates PMN via TLR2/1, resulting in the production of cytokines

24 2578 could have additional effects affecting PMN migration.

25 se to the TLR2/1 agonist, Pam3CSK4, although PMN from all donors were primed by the TLR2/6 agonist, F

26 nhibited both proteinuria and macrophage and PMN infiltration.

27 Importantly, both M-MDSCs and PMN-MDSCs showed suppression of T cell proliferation in

28 deorecorded (phase-contrast microscopy), and PMN adhesion/migration were assessed off-line.

29 regulating PMN transepithelial migration and PMN inflammatory functions.

30 ctivity; asymmetric neuronal morphology; and PMN-MN circuit motifs that could all contribute to gener

31 lood was collected for isolation of PBMC and PMN from heifers that were retrospectively classified as

32 compared between P and NP, both in PBMC and PMN.

33 inant effect on the pulmonary epithelium and PMNs.

34 ompared for different quantities of SECs and PMNs.

35 ophages was enhanced by CCL5-bound apoptotic PMN (3.6-4 fold) in a D6-dependent manner, and was essen

36 exclusively when bound to D6(+/+) apoptotic PMN.

37 receptor D6/ACKR2 is expressed on apoptotic PMN and plays an important role in regulating macrophage

38 phages when acting in concert with apoptotic PMN-expressed D6.

39 sing IL-4, IL-10, glucocorticoids, apoptotic PMNs, or azithromycin.

40 med BMM s induced efferocytosis of apoptotic PMNs compared with control BMM s.

41 ss T-cell activation, referred to by some as PMN-MDSCs, fit into this paradigm.

42 is a potent determinant of tumor-associated PMN phenotypes and direct PMN-tumor cell interactions.

43 Interactions between PMN and mycobacterial lipids impact the activation state

44 ydrate-mediated binding interactions between PMN Lewis glycans and endothelial glycan-binding protein

45 the N-linked glycan Lewis X on CD11b blocks PMN transepithelial migration (TEpM).

46 P-1 with MMP-8 and MMP-9 on peripheral blood PMN surfaces.

47 on accelerates clearance of bacteria, blunts PMN accumulation, and promotes PMN apoptosis and efferoc

48 acquisition of immunosuppressive activity by PMN-MDSCs and represents a target to inhibit the functio

49 neutrophil granulocytes (PMNs), followed by PMN apoptosis and efferocytosis.

50 B4, decreased uptake of L. monocytogenes by PMN, and inhibited the respiratory burst of PMN compared

51 perienced lethal sepsis that was reversed by PMN expansion mediated by injection of wild-type HSPCs d

52 cytosis of antibody-opsonized CLL B cells by PMNs was mediated primarily by FcgammaRIIIB in WT PMNs a

53 8/TLR13-mediated cytokine and NET release by PMNs in vitro and in vivo.

54 mans, peripheral blood frequencies of canine PMN-MDSCs and M-MDSCs are significantly higher in dogs w

55 as rhesus M-MDSCs lacked expression of CD33, PMN-MDSCs were identified as CD33(+) low-density neutrop

56 CD49d(+) PMN frequency was significantly higher in nasal lavage f

57 e sought to determine whether human CD49d(+) PMNs are present in the nasal mucosa during acute viral

58 Similar to the mouse, human CD49d(+) PMNs isolated from nasal lavage fluid during a viral res

59 In mice CD49d(+) PMNs represented a "proatopic" neutrophil subset that ex

60 ufficient to reduce accumulation of CD49d(+) PMNs in the lungs and development of postviral atopic ai

61 enotype and functional relevance of CD49d(+) PMNs.

62 lfment of apoptotic polymorphonuclear cells (PMN) during the resolution of inflammation leads to macr

63 nd peripheral blood polymorphonuclear cells (PMN).

64 phonuclear myeloid-derived suppressor cells (PMN-MDSCs) are pathologically activated neutrophils that

65 anulocytic myeloid-derived suppressor cells (PMN-MDSCs) into tumor tissues, thereby dampening the res

66 phonuclear myeloid-derived suppressor cells (PMN-MDSCs), mononuclear myeloid-derived suppressor cells

67 neutrophil myeloid-derived suppressor cells (PMN-MDSCs).

68 ed by degranulating polymorphonuclear cells (PMNs) promote pericellular proteolysis by binding to PMN

69 ion of neutrophils (polymorphonuclear cells [PMNs]) that can promote systemic spread of the infection

70 Mtb LAM did not induce any of the classical PMN priming phenotypes, including enhancement of NADPH o

71 nsfer of Gas6-depleted BMM s failed to clear PMNs in lungs following LPS challenge and mice showed se

72 ed mice more rapidly and effectively cleared PMNs in lungs compared with control BMM s.

73 CD49d and CysLTR1-coexpressing PMNs are present during symptoms of an acute viral respi

74 entified PMN-MN 'labeled line' connectivity; PMN-MN combinatorial connectivity; asymmetric neuronal m

75 In contrast, PMN recruitment to wounds infected with an isogenic AT-d

76 ng an external DC-voltage across a (011)-cut PMN-PT substrate, the ferroelectric polarization is re-o

77 METHODS AND We observed defective PMN transmigration in response to lipopolysaccharide cha

78 lammatory stimuli, and alphaMbeta2-deficient PMN displayed defective inflammatory functions.

79 f tumor-associated PMN phenotypes and direct PMN-tumor cell interactions.

80 art reflect the effects of hypoxia on direct PMN-tumor cell interactions.

81 ith cancer compared to healthy control dogs (PMN-MDSCs: p < 0.001; M-MDSCs: p < 0.01).

82 urface-bound neutrophil elastase (NE) during PMN degranulation, NE being oriented in a configuration

83 ction of cytokines but does not elicit early PMN priming responses, as seen with Pam(3)CSK(4) We spec

84 MP-8], polymorphonuclear leukocyte elastase [PMN elastase], and total protein, albumin, immunoglobuli

85 rfin (VER) was really efficient in enhancing PMN-mediated bacterial killing, while topical administra

86 y AT production and were activated to expand PMN numbers in proportion to S. aureus abundance in a ma

87 mor models, although the mechanisms favoring PMN-MDSC responses remain poorly understood.

88 potent inhibition of wound closure following PMN-MP binding to IECs.

89 that signficantly increased were assayed for PMN priming activity in vitro.

90 derived GPs had an increased ability to form PMN-MDSCs; 3) tumor-derived GPs shared gene expression p

91 Clones from PMNs and HSTMs shared a common precursor, arguably an em

92 rovide new insight into mechanisms governing PMN-induced tissue injury and implicate PMN-MPs and MPO

93 y polymorphonuclear neutrophil granulocytes (PMNs), followed by PMN apoptosis and efferocytosis.

94 mmature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adapt

95 calized with MMP-8 and -9 on activated human PMN surfaces and in PMN extracellular traps; 2) minimal

96 Here we report that mouse and human PMN-MDSCs exclusively upregulate fatty acid transport pr

97 M. tuberculosis (Mtb LAM) would prime human PMN in a TLR2-dependent manner and investigated this wit

98 etween canine and previously published human PMN-MDSC gene expression patterns.

99 We show here that primary murine and human PMNs mount a fulminant and self-propagating neutrophil e

100 ) analyses on CD11b/CD18 purified from human PMNs.

101 uate phagocytosis-induced apoptosis in human PMNs through Toll-like receptor 9 (TLR9)-mediated releas

102 Transfer of NETs to naive human PMNs prompts additional NET release, promoting further i

103 re impaired phagocytosis, and redirect human PMNs to apoptosis.

104 rapidly expressed on PMN surfaces when human PMNs are activated.

105 HUVEC: PMN co-cultures were perfused for additional 15 minutes

106 Upon relief of tumor hypoxia, PMNs were recruited less intensely to the tumor-bearing

107 of this comprehensive connectome identified PMN-MN 'labeled line' connectivity; PMN-MN combinatorial

108 ment and progression, we set out to identify PMN-MDSCs and M-MDSCs in clinical canine oncology patien

109 9-mediated endogenous mechanism that impairs PMN phagocytosis and prolongs inflammation, and demonstr

110 ning PMN-induced tissue injury and implicate PMN-MPs and MPO as important regulators of cellular func

111 nd -9 on activated human PMN surfaces and in PMN extracellular traps; 2) minimal immunoreactive and a

112 FI44, RSAD2, OAS2, LGALS3BP, IFI6 and C1R in PMN was stimulated in the P group from D18.

113 cancer progression, the role of exosomes in PMN establishment, and the function of exosomes in organ

114 dase (MPO), which is abundantly expressed in PMN azurophilic granules and is used for microbial killi

115 Overexpression of FATP2 in PMN-MDSCs was controlled by granulocyte-macrophage colon

116 r in integrin biology, with key functions in PMN trafficking during innate immunity.

117 lso identified additional conserved genes in PMN-MDSCs of multiple species that may play a role in MD

118 that FcgammaRIIIA is an important player in PMN functions, whereas FcgammaRIIIB is dispensable for a

119 est that alphaMbeta2 plays a primary role in PMN inflammatory functions and regulates the anti-inflam

120 the NLRP3 inflammasome was defective both in PMNs and in macrophages.

121 d to evolve multiple, new traits - to induce PMN inflammation and avoid adaptive immunity - to allow

122 mensal species is by their ability to induce PMN inflammation, which is dependent on the site of colo

123 red with wild-type PMNs and failed to induce PMN transmigration.

124 ally associated with amplified AMPhi-induced PMN migration into lung alveoli.

125 lial migration (P < 0.0001) and fMLP-induced PMN chemotaxis (ie, migration directionality and velocit

126 unctionally relevant receptor for MK-induced PMN recruitment as well as NET formation.

127 of this enzyme blocked S. pneumoniae-induced PMN transepithelial migration in vitro Genetic ablation

128 Intravenous (IV) succinate-induced PMN sequestration in the lung, a first event, and follow

129 -/-) mice resulted in increased WNV-infected PMN infiltration and viral burden in the brain, which wa

130 WNV neuroinvasion by recruiting WNV-infected PMNs into the brain.

131 ere proteinuria, few glomerulus-infiltrating PMN were found, leaving macrophages and, to a less exten

132 croparticles released by tissue infiltrating PMNs (PMN-MPs) serve as shuttles to protect and deliver

133 hanism whereby activated tissue-infiltrating PMNs release microparticles armed with proinflammatory m

134 hway of myeloid differentiation to influence PMN-MDSC production has remained unknown.

135 We show that C-sep isolated PMNs show higher neutrophil elastase (NE) release follow

136 t inhibit TEpM and differentially affect key PMN inflammatory functions including phagocytosis, super

137 le of these macrophages but not the PD-L1(-) PMN in GN development and in inducing podocyte damage.

138 ion by reducing polymorphonuclear leukocyte (PMN) recruitment to the affected organs.

139 collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and pro

140 overs 94.0% of polymorphonuclear leukocytes (PMNs), with up to 10(5) PMNs in clear diluted buffer fro

141 f neutrophils (polymorphonuclear leukocytes [PMN]), macrophages (MPhi), Langerin(+) dendritic cells (

142 n neutrophils (polymorphonuclear leukocytes [PMNs]) generate inflammatory responses within the joints

143 xosome) to improve drug delivery to the lung PMN.

144 re-routed M-MDSC, but not granulocytic-MDSC (PMN-MDSC), into cells that elicited direct antitumor cyt

145 al networks, including the posterior-medial (PMN) and the anterior-temporal (ATN) networks.

146 KO) mice were resistant to antibody-mediated PMN-dependent TRALI induction.

147 a Helicobacter pylori mouse infection model, PMN infiltration into the gastric mucosa is dramatically

148 endotoxemia, we developed a new mouse model, PMN(DTR) mice, in which injection of diphtheria toxin in

149 important means of therapeutically modifying PMN-mediated vascular inflammation.

150 mp-8 and Mmp-9 share binding sites on murine PMN surfaces.

151 imp-1 (but not Timp-2) to Timp-1(-/-) murine PMNs reconstitutes the binding of exogenous pro-Mmp-8 an

152 the surface of activated Timp-1(-/-) murine PMNs; and 3) binding of exogenous Timp-1 (but not Timp-2

153 ail to bind to Mmp-8(-/-)x Mmp-9(-/-) murine PMNs.

154 d pro-Mmp-9 to Mmp-8(-/-)x Mmp-9(-/-) murine PMNs.

155 r binding to membrane-bound Timp-1 on murine PMNs.

156 rituximab in primary membranous nephropathy (PMN) have not been conducted.

157 ving tumor hypoxia thus greatly improved net PMN-dependent tumor control, leading to a massive reduct

158 ment of all 60 MNs and 236 premotor neurons (PMNs), including differentially-recruited MNs.

159 Neutrophil (PMN) infiltration of the intestinal mucosa is a hallmark

160 Neutrophil (PMN) infiltration of the intestinal mucosa often leads t

161 monstrated the requirement for a neutrophil (PMN) subset expressing CD49d to drive development of pos

162 , WNV-infected polymorphonuclear neutrophil (PMN) infiltration and viral burden in brain of Opn (-/-)

163 mmatory skin disease with strong neutrophil (PMN) infiltration and high levels of the antimicrobial p

164 thelium and on polymorphonuclear neutrophil (PMNs) after transepithelial migration into the alveolar

165 crophages and polymorphonuclear neutrophils (PMN) are important in inducing GN, as anti-CD11b and -IC

166 Because polymorphonuclear neutrophils (PMN) interaction with ECs generates reactive oxygen spec

167 ecruitment of polymorphonuclear neutrophils (PMN) to bacterial and fungal pathogens as well as to mod

168 al killing by polymorphonuclear neutrophils (PMN) using a mouse model of foodborne listeriosis.

169 Efferocytosis of apoptotic neutrophils (PMNs) by alveolar macrophages (AM s) is vital for resolu

170 ted decreased survival in human neutrophils (PMNs) as compared with the parent, while YpdA overexpres

171 the pulmonary sequestration of neutrophils (PMNs), which serves as the first event in the acute resp

172 Polymorphonuclear neutrophils (PMNs) are increasingly recognized to influence solid tum

173 filtration of polymorphonuclear neutrophils (PMNs) but also reduces fibrosis and preserves systolic f

174 rafficking of polymorphonuclear neutrophils (PMNs) during inflammation critically depends on the beta

175 observed that polymorphonuclear neutrophils (PMNs) from FcgammaRIIIB wild-type (WT) individuals or th

176 ecruitment of polymorphonuclear neutrophils (PMNs) from the bone marrow via the circulation and local

177 Polymorphonuclear neutrophils (PMNs) from these KO mice had defective innate immune res

178 Polymorphonuclear neutrophils (PMNs) have previously been reported to mediate phagocyto

179 Polymorphonuclear neutrophils (PMNs) play a critical role in the innate immune response

180 neutrophils (polymorphonuclear neutrophils [PMNs]) are considered to be the major pathogenic cells.

181 ent in the configuration Terfenol-D/CoFeB/Ni/PMN-PT wherein one desired mode exhibits a much higher t

182 PT with Cu as spacer and Terfenol-D/CoFeB/Ni/PMN-PT.

183 nvestigated by a modeling approach, Ni/Ni/Ni/PMN-PT with Cu as spacer and Terfenol-D/CoFeB/Ni/PMN-PT.

184 organs is crucial for pre-metastatic niche (PMN) formation and metastasis.

185 The pre-metastatic niche (PMN) is an environment in a secondary organ conducive to

186 ip between primary mediastinal nonseminomas (PMNs) and hematologic somatic-type malignancies (HSTMs).

187 -opsonized beads by FcgammaRIIIB WT and null PMNs.

188 aRIIIB in WT PMNs and by FcgammaRIIA in null PMNs.

189 PGE(2) pretreatment decreased the ability of PMN harvested from the bone marrow of either BALB/cByJ o

190 nhibition of FATP2 abrogated the activity of PMN-MDSCs and substantially delayed tumour progression.

191 FATP2 abrogated the suppressive activity of PMN-MDSCs.

192 The enzymatic activity of PMN-MP-associated MPO was enhanced compared with soluble

193 PMN, and inhibited the respiratory burst of PMN compared with vehicle-treated cells.

194 However, exposure of PMN to Mtb LAM did elicit pro- and anti-inflammatory cyt

195 resents a target to inhibit the functions of PMN-MDSCs selectively and to improve the efficiency of c

196 tail of CD18 and is crucial for induction of PMN adhesion and postadhesion events, including adhesion

197 Importantly, localized microinjection of PMN-MPs into wounded colonic mucosa was sufficient to im

198 oteins are critical for initial migration of PMN out of the vasculature.

199 PGE(2) treatment slowed the migration of PMN toward the chemoattractant leukotriene B4, decreased

200 n parallel, CORM-401-dependent modulation of PMN chemotaxis, F-actin expression/distribution, and act

201 We investigated modulation of PMN-endothelial cell adhesive interactions by water-solu

202 ipulation of CD11b function and reduction of PMN-associated tissue damage in chronic inflammatory dis

203 We focus on regulation of PMN number and function and the role of pore-forming alp

204 The transcriptomic signatures of PMN-MDSCs and M-MDSCs are distinct, and moreover reveal

205 and provides insights into the structure of PMN that require rethinking its existing contentious mod

206 Transition of PMN rolling to firm adhesion critically depends on Coro1

207 pite recent advances in the understanding of PMN-MDSC biology, the mechanisms responsible for the pat

208 b, we observed that a mean of 50% and 75% of PMNs had taken a fraction of the dye from CLL B cells at

209 cies and histone release after activation of PMNs, along with defective phagocytosis.

210 mucosa decreased the detrimental effects of PMNs and enhanced tissue healing responses, suggesting t

211 The pathological effects of PMNs are largely attributed to the release of soluble me

212 ype transition resulting in efferocytosis of PMNs plays a crucial role in the resolution of inflammat

213 Live imaging of PMNs showed that MRS2578 represses neutrophil migration

214 includes a robust inflammatory infiltrate of PMNs and macrophages.

215 e mechanism of transendothelial migration of PMNs.

216 d suggest that the contrasting properties of PMNs in different tumor settings may in part reflect the

217 However, dysregulated mucosal trafficking of PMNs and associated epithelial tissue damage is a pathol

218 Thus, endotoxin-induced transmigration of PMNs was secondary to TRPM2-activated Ca(2+) signaling a

219 tor of soluble MMPs) is rapidly expressed on PMN surfaces when human PMNs are activated.

220 tric structure with Pt/Co/Ni/Co/Pt layers on PMN-PT substrate.

221 presence and role of FcgammaRIIIA (CD16A) on PMNs.

222 ceptor CD44, interleukin 6 (IL-6), and other PMN chemoattractants including macrophage inflammatory p

223 2Nb1/2)O3-(y)Pb(Mg1/3Nb2/3)O3-(x)PbTiO3 (PIN-PMN-PT) crystals under high strain rate loading.

224 The obtained results indicate that PIN-PMN-PT crystals became completely depolarized under 3.9

225 ticles released by tissue infiltrating PMNs (PMN-MPs) serve as shuttles to protect and deliver active

226 t monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs can be detected using several of the markers

227 or subsets, monocytic and polymorphonuclear (PMN).

228 on but also accumulate in polymorphonuclear (PMN) cells.

229 ified in humans and mice: polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs.

230 Neutrophils, polymorphonuclear (PMN) leukocytes, play an important role in the early inn

231 SECs) and high numbers of polymorphonuclear (PMN) cells are regarded as indicative of a lower respira

232 CXCR7 antagonism reduced the most potent PMN chemoattractants CXCL1 and CXCL2/3.

233 (or inactive compound iCORM-401)-pretreated PMN for 5 minutes in the presence of 1.0 dyn/cm(2) shear

234 Pretreating PMN with CORM-401 did not suppress PMN adhesion to HUVEC

235 P-ribose polymerase in ECs of mice prevented PMN transmigration.

236 ulate that the inability of Mtb LAM to prime PMN may be due to differential localization of TLR2/1 si

237 d assay if these increased metabolites prime PMNs and induce pulmonary sequestration in an animal mod

238 The metabolites that primed PMNs were tested in a two-event animal model of ARDS to

239 r (SUCNR1) inhibition abrogated PMN priming, PMN sequestration, and ARDS.

240 teria, blunts PMN accumulation, and promotes PMN apoptosis and efferocytosis, thereby facilitating re

241 nflammation, probably via MK, which promotes PMN trafficking and NETosis.

242 is involved in TRALI induction by promoting PMN recruitment to the lungs.

243 1 plays a counterintuitive role in promoting PMN pericellular proteolysis occurring in chronic obstru

244 Patients with biopsy-proven PMN and nephrotic syndrome after 6 months of nonimmunosu

245 r, restored the TRALI response and pulmonary PMN accumulation.

246 on to the lungs and stimulation of pulmonary PMN recruitment.

247 ect any significant phagocytosis by purified PMNs of anti-CD20-opsonized CLL B cells, but could detec

248 alone were able to activate highly purified PMNs from the FcgammaRIIIB-null donor.

249 hed the intraocular inflammation and reduced PMN infiltration in mouse eyes, but, increased the bacte

250 h wild-type S. aureus enriched in AT reduced PMN recruitment and resulted in sustained bacterial burd

251 induced by LPS, C6(-/-) mice showed reduced PMN buildup and less lung epithelial/endothelial cell dy

252 adhesion to HUVEC, but significantly reduced PMN transendothelial migration (P < 0.0001) and fMLP-ind

253 18 plays a well-described role in regulating PMN transepithelial migration and PMN inflammatory funct

254 nd event, resulted in ARDS in vivo requiring PMNs.

255 3) value for the [001]-oriented rhombohedral PMN-PT crystals, challenging the conventional wisdom tha

256 Sm-doped Pb(Mg(1/3)Nb(2/3))O(3)-PbTiO(3) (Sm-PMN-PT) single crystals with even higher d (33) values r

257 We characterized the Sm-PMN-PT on the atomic scale with scanning transmission el

258 Importantly, such PMN-derived exosomes exist in clinical specimens from su

259 t that robust PGE(2) production can suppress PMN effector functions, leading to decreased bacterial k

260 etreating PMN with CORM-401 did not suppress PMN adhesion to HUVEC, but significantly reduced PMN tra

261 pharmacologic inhibition of NLRP3 suppressed PMN-MDSC tumor infiltration and significantly augmented

262 e of Escherichia coli in mice and suppresses PMN apoptosis, efferocytosis, and generation of proresol

263 Surprisingly, PMN from only a subset of donors were primed in response

264 These findings support the hypothesis that PMN-MDSCs result from selective expansion of IRF8(lo) GP

265 This model predicts that PMN inflammation produces the serious sequelae of gonorr

266 itro and in vivo injury models, we show that PMN-derived miR-23a and miR-155 promote accumulation of

267 ow cytometry, and western blot analysis that PMNs from FcgammaRIIIB WT donors and the null individual

268 We conclude that PMNs mediate mostly trogocytosis rather than phagocytosi

269 However, recent data have suggested that PMNs, like macrophages, can also mediate trogocytosis.

270 The PMN receptor(s) to which MMP-8 and MMP-9 bind(s) is not

271 r of switchable ferroelastic strain from the PMN-PT substrate into the epitaxially grown V(2)O(3) fil

272 (12-LOX), which is required to generate the PMN chemoattractant hepoxilin A3 (HXA3) from arachidonic

273 Membrane-bound TIMP-1 is the PMN receptor for pro- and active MMP-8 and -9 as shown b

274 rection of the applied electric field on the PMN-PT substrate, which fully replaces the controllabili

275 DSC burden in tumor models, particularly the PMN-MDSC subset.

276 Succinate alone primed the PMN oxidase in vitro at physiologically relevant levels.

277 ticipants received stimulation targeting the PMN or an out-of-network control location.

278 al killing, was found to be mobilized to the PMN surface and subsequently released in association wit

279 achieved with applied electric field to the PMN-PT [011] substrate.

280 retrieval task versus during rest within the PMN and the ATN.

281 iographical retrieval versus rest within the PMN.

282 used to construct phylogenetic trees of the PMNs and the ensuing HSTM clones.

283 iple distinct clones not detected within the PMNs.

284 This PMN-MN connectome will provide a foundation for analyzin

285 act infections and further characterize this PMN subset in human subjects and mice.

286 By anchoring MMP-8 and MMP-9 to PMN surfaces, membrane-bound TIMP-1 plays a counterintui

287 omote pericellular proteolysis by binding to PMN surfaces in a catalytically active tissue inhibitor

288 to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement prote

289 ficantly reduced Ca(2+) entry in response to PMN activation of TRPM2 in ECs.

290 inhibition of CXCR7 reduced transepithelial PMN migration by affecting the expression of adhesion mo

291 in ECs via TRPM2 as compared with wild-type PMNs and failed to induce PMN transmigration.

292 ly released in association with PMN-MPs upon PMN activation and binding to intestinal epithelial cell

293 regulated molecular mechanisms through which PMNs directly induce tumor cell death and proliferation

294 nd subsequently released in association with PMN-MPs upon PMN activation and binding to intestinal ep

295 were perfused for additional 15 minutes with PMN-free medium containing CORM-401/inactive CORM-401.

296 d with elevated salivary aMMP-8 but not with PMN elastase.

297 analysis of a large cohort of patients with PMNs also demonstrated a high prevalence of TP53 mutatio

298 These data likely explain why patients with PMNs are frequently resistant to platinum-based chemothe

299 e discrimination of IPMN from SCN and within PMNs predict the grade of dysplasia.

300 was mediated primarily by FcgammaRIIIB in WT PMNs and by FcgammaRIIA in null PMNs.