ライフサイエンスコーパス: NET

1 NET release was quantified using a High-Content Imaging

2 NETs (~90 nm diameter) were fabricated from hemoglobin-d

3 NETs are composed of nuclear DNA-derived web-like struct

4 NETs formed a barrier "dead zone," confining bacteria to

5 NETs thus furnish a previously unsuspected link between

6 NETs were detected in the omentum of ovarian tumor-beari

7 NETs were found in the airway compartment and neutrophil

8 NETs wrap and coat tumor cells and shield them from cyto

9 NETs, in turn, bound ovarian cancer cells and promoted m

10 psy, n = 46; GNETs Type 1: 42 (32 NET G1, 10 NET G2), a GNET Type 3: 1 well-differentiated NET G3, ne

11 hybrid clone RA015/11.88 and RA056/11.23.2, NET and/or cit-H2B immunoreactivity was solely dependent

12 NENs at biopsy, n = 46; GNETs Type 1: 42 (32 NET G1, 10 NET G2), a GNET Type 3: 1 well-differentiated

13 T/CT scans from 21 healthy volunteers and 42 NET-positive patients to determine those with disease or

14 rophils promoted ATC cell proliferation in a NET-dependent manner.

15 We discuss prior reports linking aberrant NET formation to pulmonary diseases, thrombosis, mucous

16 6-fold higher PA signal from the accumulated NETs in the coronary artery above the ligation.

17 morphologically a net, rendering the acronym NETs particularly appropriate.

18 NETs to naive human PMNs prompts additional NET release, promoting further inflammation.

19 an synovial tissues frequently react against NETs.

20 Higher levels of airway NETs are associated with fewer ventilator-free days.

21 of neutrophil degranulation, activation and NET release were found in children with versus without P

22 ll IFN signaling, neutrophil activation, and NET production is associated with PARDS.

23 humans that regulates protease activity and NET formation and modifies efferocytosis.

24 gnificantly reduced platelet aggregation and NET release.

25 Changes in the proteome, granule content and NET formation also occurred in human neutrophils, and co

26 7 triggered TLR8/TLR13-mediated cytokine and NET release by PMNs in vitro and in vivo.

27 H-induced regional variations in the DAT and NET-enriched FC maps were significantly correlated with

28 synovial B cell clones reactive to NETs and NET-derived Ags such as citrullinated histones.

29 ng to chronic inflammation in psoriasis, and NET-associated RNA (naRNA) as a physiologically relevant

30 endothelial injury, platelet retention, and NET release in conditions where antibodies trigger these

31 pecimens, cell-based inhibition studies, and NET/human aortic endothelial cell (HAEC) cocultures.

32 otic clinical presentations in COVID-19, and NETs may represent targets for therapeutic intervention.

33 c basis for a pivotal role of complement and NETs in COVID-19 immunothrombosis.

34 raction of NETs with macrophages or DCs, and NETs alone were found to be noninflammatory, whereas imm

35 ement depletion reduced both lung injury and NETs.

36 dence for the involvement of neutrophils and NETs, to weigh the implications, and to increase efficie

37 Anti-NET/cit-H2B immunoreactivity of selected RA-rmAbs was ab

38 RhADAMTS13 and anti-NET treatments could be new therapeutic strategies to pr

39 Furthermore, novel anti-NET therapies are being developed which may have profoun

40 ion sites are observed in a minority of anti-NET B cell clones but can strongly influence NET-Ag bind

41 Selected anti-NET RA-rmAbs derived from synovial RA CD19(+) B cells we

42 ylation mutants (N->Q) and analyzed for anti-NETs and citrullinated histones (cit-H2B) immunoreactivi

43 Appendiceal NETs are usually diagnosed accidentally after appendecto

44 y related to nodal metastases in appendiceal NETs.

45 underwent surgical resection of appendiceal NETs at 11 tertiary Italian centers, from January 1990 t

46 SPs play no role in either NETosis or arming NETs with proteolytic activity.

47 Thus, MK as well as NETs may represent novel therapeutic targets for the tre

48 We assessed NET formation ex vivo in COVID-19 neutrophils and in hea

49 NET formation in vitro, not only attenuates NET formation in vivo and the infiltration of polymorpho

50 19 platelet-rich plasma generated TF-bearing NETs that induced thrombotic activity of HAECs.

51 We studied the connection between NETs and COVID-19 severity and progression.

52 dings shed light on the interactions between NETs and phagocytic cells and provide new insights regar

53 onatal NET-inhibitory factor (nNIF) to block NET formation induced by COVID-19 plasma.

54 Inhibition of actin disassembly blocked NET release.

55 Tumor cells protected from cytotoxicity by NETs underlie successful cancer metastases in mice and t

56 TC cells to determine the effects exerted by NETs on cell proliferation.

57 response, but independently of the canonical NET component, DNA.

58 ration significantly diminished plasma cfDNA/NETs levels.

59 rmation) or DNase 1 treatment (which cleaves NETs) also prolonged allograft survival.

60 let-associated chemokine, binds and compacts NETs, increasing their resistance to DNase I.

61 plasma myeloperoxidase (MPO)-DNA complexes (NETs), platelet factor 4, RANTES, and selected cytokines

62 COVID-19, and pulmonary autopsies confirmed NET-containing microthrombi with neutrophil-platelet inf

63 Consistently, NETs are present in necrotic lung lesions of TB patients

64 Moreover, the NSPs that decorate NETs are in an inactive conformation and thus cannot par

65 ophils being rapidly recruited and deploying NETs around skin-penetrating larvae.

66 96.6% specificity (P < 0.0001) for detecting NETs, which translated to a 100.0% sensitivity and 96.8%

67 ET G2), a GNET Type 3: 1 well-differentiated NET G3, neuroendocrine carcinomas (NECs) (n = 3), and co

68 riptional regulator of poorly differentiated NETs.

69 d that coagulation may be enhanced by direct NET-dependent activation of the contact system.

70 hould continue to be considered the dominant NET in IPCC and other scenarios achieving the Paris targ

71 cluded, 39 had metastasis at diagnosis of DP-NET, 50 developed metastases during follow-up, and 69 di

72 DP-NETs of 2 cm in size or more, regardless of the associat

73 DP-NETs, with their numerous lesions and endocrine secretio

74 ival of patients with large nonfunctional DP-NETs is known to be poor, but the overall contribution o

75 be poor, but the overall contribution of DP-NETs to metastatic spread is poorly known.

76 e study population included patients with DP-NETs diagnosed after 1990 and followed in the MEN1 cohor

77 Treatments that enhance NET degradation may liberate captured bacteria and toxic

78 cated decreased mTOR signalling and enhanced NET-1 expression in both cell lines, and (18)F-mFBG reve

79 kworm, Necator americanus, which also evaded NETs in vitro.

80 For example, NETs initiate excessive deposition of collagen, resultin

81 Excessive NET formation has been implicated in several noninfectio

82 D-19 neutrophils ex vivo displayed excessive NETs at baseline, and COVID-19 plasma triggered NET form

83 and fluorescence in vivo imaging by exciting NETs at 800 nm and 650 nm, respectively.

84 In these experiments, NET-resident histone H2a attracted monocytes in a recept

85 Tate and PARP inhibition in SSTR2-expressing NET.

86 for the detection of somatostatin-expressing NETs.

87 e III study of patients with SSTR-expressing NETs.

88 transcript-cap analysis of gene expression (NET-CAGE), to sensitively detect 5' ends of nascent RNAs

89 Finally, NETs released by SARS-CoV-2-activated neutrophils promot

90 arginine deiminase 4 (PAD4, a key enzyme for NET formation) or DNase 1 treatment (which cleaves NETs)

91 ) citrullinates histones and is required for NET formation (NETosis) in mouse neutrophils.

92 ee COVID-19 lung autopsies were examined for NETs and platelet involvement.

93 n the management and surveillance of gastric NET disease.

94 atients with 24 histologically confirmed GEP NET lesions (15 men and 7 women; median age, 61 y; range

95 ferentiation between grade 1 and grade 2 GEP NETs.

96 tion between low- and intermediate-grade GEP NETs.

97 atients with 24 histologically confirmed GEP-NET lesions (15 men/7 women; median, 61 years, range, 43

98 A total of 854 patients with GI-NET metastases on presentation underwent 392 PTRs.

99 Ki-67 indices for 50 GI-NETs were quantitated using SKIE and compared with DS sl

100 e accuracy of Ki-67 index quantitation in GI-NETs: (1) Synaptophysin-KI-Estimator (SKIE), a pipeline

101 n gastrointestinal neuroendocrine tumors (GI-NETs) and defines tumor grade.

102 igation of myeloid cell infiltration in HCC, NET and intrahepatic CCA tumors further established that

103 Higher NETs were detected in the airways of children with venti

104 Methods: Human NET cell lines BON1 and QGP1 were treated with 5-fluorou

105 Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target

106 Our findings implicate NET formation in rendering the premetastatic omental nic

107 alized series of reactions that culminate in NET formation.

108 vealed a concentration-dependent increase in NET-1 function.

109 TATOC tumor uptake predict better outcome in NET patients treated with (90)Y-DOTATOC.

110 Unexpectedly, RNA, which is abundant in NETs and psoriatic but not healthy skin, in complex with

111 y of 95% for predicting responses to PRRT in NETs.

112 e persistence of biofilm bacteria trapped in NETs is facilitated by S. aureus nuclease (Nuc)-mediated

113 ion in neutrophils, leading to the increased NET formation via Rho activation to exaggerate inflammat

114 We now show that PF4 increases NET-mediated bacterial capture, reduces the release of N

115 ATC CM induce NET release, whereas papillary TC or normal thyroid CM d

116 ATC CM-induced NET production occurred in a reactive oxygen species-dep

117 f Rho significantly decreased rmCIRP-induced NET formation in BMDN.

118 mine the mitochondrial origin of ATC-induced NETs.

119 eport a novel link between airway infection, NET formation, and disease severity in bronchiectasis du

120 NET B cell clones but can strongly influence NET-Ag binding.

121 Therefore, interventions that inhibit NET release would likely be ineffective at preventing NE

122 did not significantly modulate intratumoural NET-1 activity.

123 Mechanistically, NETs triggered by SARS-CoV-2 depend on angiotensin-conve

124 telet-neutrophil crosstalk, mechanosensitive NET production, and provide mechanistic insight into the

125 C5aR1 blockade attenuated platelet-mediated NET-driven thrombogenicity.

126 ng the cytokine midkine (MK), which mediates NET formation in vitro, not only attenuates NET formatio

127 Recapitulating the observations in mice, NETs were also observed in all the examined allografts f

128 German motor neuron disease centers (ALS/MND-NET).

129 We also tested the ability of neonatal NET-inhibitory factor (nNIF) to block NET formation indu

130 l microscopy provides evidence of neutrophil NETs interfering cytolytic cytotoxic T lymphocytes (CTLs

131 in murine sepsis models, supporting a novel NET-targeting approach to improve outcomes in sepsis.

132 ect of injectable norethisterone oenanthate (NET-EN), combined contraceptive vaginal rings (CCVR; Nuv

133 s and raise the possibility that blockade of NET formation prevents omental metastasis.

134 ureus nuclease (Nuc)-mediated degradation of NET DNA.

135 ical management and enable identification of NET-inducing factors in individual patients for targeted

136 Inhibition of NET formation in experimental autoimmune myocarditis (EA

137 along the arterial lumen, and inhibition of NET release annulled lesion expansion during endotoxinem

138 l biology, the triggers to and mechanisms of NET formation, and the contribution of NETs to atheroscl

139 In vitro, IL-17A was a potent promoter of NET formation.

140 frequencies to a greater extent than use of NET-EN or COCPs, although Th17 cells were more activated

141 The DNA backbone of NETs not only presents intrinsic neutrophil proteins (eg

142 ogic changes, suggesting biocompatibility of NETs.

143 vide new insights regarding the clearance of NETs, double-edged swords of innate immunity.

144 The concentration of NETs was augmented in plasma, tracheal aspirate, and lun

145 ms of NET formation, and the contribution of NETs to atherosclerosis and to thrombosis.

146 accharide treatment led to the deposition of NETs along the arterial lumen, and inhibition of NET rel

147 WF), interacts with the extracellular DNA of NETs to potentially immobilize them during inflammatory

148 , larvae were able to mitigate the effect of NETs by secreting a deoxyribonuclease (Nb-DNase II) to d

149 (NE) has been implicated in the formation of NETs through proteolysis of nuclear proteins leading to

150 enzymes is not required for the formation of NETs.

151 While the in vivo impact of NETs is accumulating, the cellular events driving NETosi

152 fect of ADAMTS13 treatment and the impact of NETs on skin allografts, however, remain unexplored.

153 Therefore, the inhibition of NETs represents a potential therapeutic target for COVID

154 is study, we investigated the interaction of NETs released by freshly isolated, PMA-stimulated primar

155 multiplex array following the interaction of NETs with macrophages or DCs, and NETs alone were found

156 tudy aimed to investigate the involvement of NETs in human TC.

157 Increased plasma levels of NETs, tissue factor (TF) activity, and sC5b-9 were detec

158 their neutrophils released higher levels of NETs.

159 We consider the use of markers of NETs in clinical studies.

160 rescence microscopy revealed the presence of NETs in allografts of vehicle, but surprisingly, not in

161 We report the presence of NETs in the lungs of each COVID-19 patient.

162 urrent knowledge on the molecular profile of NETs and the strategies and tools used to predict, monit

163 ith rmCIRP resulted in reduced quantities of NETs compared to WT rmCIRP-treated neutrophils.

164 ARS-CoV-2 can directly induce the release of NETs by healthy neutrophils.

165 Airway fluid was analyzed for the release of NETs by myeloperoxidase-DNA complexes using an ELISA.

166 swarms against Candida, but their release of NETs is delayed, resulting in impaired control of fungal

167 o antibiotic therapy, supporting the role of NETs in a late stage of TB pathogenesis.

168 sults unravel a possible detrimental role of NETs in the pathophysiology of COVID-19.

169 we provide an updated review on the role of NETs in the perioperative period with specific emphasis

170 keletal muscle, however, direct targeting of NETs via the peptidylarginine deiminase 4 (PAD4) mechani

171 Transfer of NETs to naive human PMNs prompts additional NET release,

172 150 uL of NETs (20 uM ICG,) was IV injected via tail vein 1-hour p

173 mporal information on protease activities on NETs is available in a pathophysiological context to dat

174 Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a s

175 t crossover, CCVR users changing to COCPs or NET-EN did not resolve activation or cytokines, although

176 Neutrophils depletion or NET inhibition altered larvae behavior and enhanced the

177 Through pan-NET analyses, we identified ONECUT2 as a candidate maste

178 (eg, ATM and DAXX) are limited to pancreatic NETs and are most likely not informative.

179 A monoclonal antibody KKO which binds to PF4-NET complexes, further enhances DNase resistance.

180 se would likely be ineffective at preventing NET-based injury.

181 of the (123)I-mIBG radiotracer, to quantify NET-1 expression levels in mouse models of NB following

182 ibitor of TLR7/8/9, following injury reduced NET formation, IL-10, and TNFalpha levels and ultimately

183 ssens inflammation in allografts by reducing NET burden, resulting in enhanced allograft survival.

184 owing body of clinical information regarding NETs.

185 ents yielded high TF expression and released NETs carrying active TF.

186 ed RNA (naRNA) as a physiologically relevant NET component.

187 lts diagnosed with synchronous metastatic SB-NET between 2001-2017 in Ontario.

188 all bowel resection (USBR) for metastatic SB-NET compared to non-operative management (NOM) on long-t

189 in metastatic small bowel neuroendocrine (SB-NET) remains controversial.

190 USBR for SB-NETs in the presence of metastatic disease was associate

191 USBR should be considered for metastatic SB-NETs.

192 ing native elongating transcript sequencing (NET-seq) to yeast cells, we show that Xrn1 functions mai

193 roteasome system in suppression of p27 in SI-NET, and inhibition of neddylation as a putative therape

194 ion as a putative therapeutic strategy in SI-NET.

195 sentation, patients often have a significant NET burden contributing to the multiorgan damage.

196 We propose that interventions that stabilize NETs and sequester NDPs may be protective in sepsis.

197 If our hypothesis is correct, targeting NETs directly and/or indirectly with existing drugs may

198 erred to as negative emissions technologies (NETs), is the production and combustion of bioenergy cro

199 ncies were significantly higher in CCVR than NET-EN and COCP.

200 Our study shows that NET-associated histone H2a mediates charge-dependent mon

201 y complications of COVID-19 and suggest that NET-targeting approaches could be considered for the tre

202 discover that NETs shield tumor cells from cytotoxic immune cells, res

203 Our results support the hypothesis that NETs may represent drivers of severe pulmonary complicat

204 s in psoriatic lesions, we hypothesized that NETs contribute to increased T helper type 17 (Th17) cel

205 Multiple studies have since shown that NETs play a role in tumor progression and metastasis.

206 We have previously shown that NETs trap tumor cells in both the liver and the lung, in

207 n during endotoxinemia, thus suggesting that NETs regulate myeloid cell recruitment.

208 In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecul

209 loss of granule content and reduction of the NET-forming capacity.

210 TAT is a dual-targeting agent, targeting the NET function and the thyrointegrin alphavbeta3 receptors

211 rial reactive oxygen species production; the NETs contained mitochondrial DNA.

212 allergic donor serum in vitro impaired their NET formation and migration toward CXCL8, thereby mirror

213 wever, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the

214 Methods: Forty-three NET patients received up to 4 cycles of (90)Y-DOTATOC at

215 oxidase, and restricts fungal growth through NET release within the swarm.

216 Thus, NETs triggering immunothrombosis may, in part, explain t

217 15-19 years) were randomly assigned 1:1:1 to NET-EN, CCVR, or COCPs for 16 weeks, then subsequently c

218 er FSH and LH concentrations, as compared to NET-EN and COCPs, with FSH concentrations and Th17 frequ

219 lower FHS and LH concentrations compared to NET-EN/COCPs, with FHS concentrations and Th17 frequenci

220 her nuclei or mitochondria can contribute to NET formation.

221 lls is necessary for the immunoreactivity to NET-Ags.

222 diates charge-dependent monocyte adhesion to NETs and accelerates atherosclerosis during endotoxinemi

223 study the mechanism of monocyte adhesion to NETs, we used in vitro adhesion assays and biophysical a

224 elastase (NE) and cathepsin G (CG) attach to NETs and contribute to the diverse immune outcome.

225 ion in RA synovial B cell clones reactive to NETs and NET-derived Ags such as citrullinated histones.

226 ion may liberate captured bacteria and toxic NET degradation products (NDPs) and likely be of limited

227 ar-infrared erythrocyte-derived transducers (NETs), a contrast agent, in combination with a photoacou

228 targeting of the norepinephrine transporter (NET) function with benzylguanidine (BG), conjugated with

229 er (DAT) and the norepinephrine transporter (NET), to unravel its effects on dopaminergic and noradre

230 ate of the human norepinephrine transporter (NET-1), shows promising responses in heavily pre-treated

231 f-propagating neutrophil extracellular trap (NET) and cytokine response, but independently of the can

232 n with robust neutrophil extracellular trap (NET) formation in the skeletal muscle, however, direct t

233 I IFN-induced neutrophil extracellular trap (NET) formation that promotes bacterial growth and promot

234 ifferences in neutrophil extracellular trap (NET) formation, oxidized mitochondrial DNA release, chem

235 escription of neutrophil extracellular trap (NET) release by activated neutrophils, some animal model

236 regation, and neutrophil extracellular trap (NET) release in the liver.

237 es, including neutrophil extracellular trap (NET) release, were intact in endothelial MHC I-deficient

238 wed that anti-neutrophil extracellular trap (NET) rheumatoid arthritis (RA)-rmAbs derived from CD19(+

239 Although neutrophil extracellular DNA traps (NETs) entrap and kill pathogens, they also contribute to

240 aureus biofilms produce extracellular traps (NETs) and phagocytose bacteria, both mechanisms are inef

241 Neutrophil extracellular traps (NETs) are elevated in adults with ARDS.

242 A (eDNA) and neutrophil extracellular traps (NETs) are implicated in multiple inflammatory diseases.

243 Neutrophil extracellular traps (NETs) are web-like DNA structures decorated with histone

244 Neutrophil extracellular traps (NETs) can contribute to inflammation-associated lung dam

245 Neutrophil extracellular traps (NETs) can promote tumor growth and metastases, but wheth

246 s, releasing neutrophil extracellular traps (NETs) composed of DNA complexed with histones and toxic

247 Neutrophil extracellular traps (NETs) composed of nuclear DNA associated with histones a

248 Neutrophil extracellular traps (NETs) consist of DNA released by terminally stimulated n

249 idering that neutrophil extracellular traps (NETs) have been described as important mediators of tiss

250 r discovery, neutrophil extracellular traps (NETs) have been implicated in a broad array of functions

251 presence of neutrophil extracellular traps (NETs) have been implicated in liver and lung allograft f

252 Neutrophil extracellular traps (NETs) have recently emerged as a newly recognized contri

253 of increased neutrophil extracellular traps (NETs) in diabetic wounds.

254 Neutrophil extracellular traps (NETs) originate from decondensed chromatin released to i

255 ream to form neutrophil extracellular traps (NETs) that confine and kill circulating pathogens.

256 formation of neutrophil extracellular traps (NETs) was reduced in affected cells (p = 0.015), and pha

257 d release of neutrophil extracellular traps (NETs), a meshwork of decondensed chromatin lined with hi

258 ls, triggers neutrophil extracellular traps (NETs), and excludes cytotoxic CD8 T cells from tumors.

259 by releasing neutrophil extracellular traps (NETs), but whether they target hookworms during skin inf

260 lity to form neutrophil extracellular traps (NETs)-may contribute to organ damage and mortality in CO

261 e release of neutrophil extracellular traps (NETs).

262 s and DNA as neutrophil extracellular traps (NETs).

263 formation of neutrophil extracellular traps (NETs).

264 a release of neutrophil extracellular traps (NETs).

265 resulting in neutrophil extracellular traps (NETs).

266 discharge of neutrophil extracellular traps (NETs).

267 xtrude their neutrophil extracellular traps (NETs).

268 e amounts of neutrophil extracellular traps (NETs).

269 the platelet/neutrophil extracellular traps (NETs)/thrombin axis, using COVID-19 specimens, cell-base

270 s at baseline, and COVID-19 plasma triggered NET formation, which was blocked by nNIF.

271 Soluble and cellular factors triggering NETs were significantly increased in COVID-19, and pulmo

272 biopsy has utility in neuroendocrine tumor (NET) diagnosis and identification of residual disease.

273 lide therapy (PRRT) in neuroendocrine tumor (NET) patients treated with (90)Y-DOTATOC in the setting

274 luding non-viral HCC, neuroendocrine tumors (NET), and colorectal carcinoma with liver metastases (CR

275 vement in appendiceal neuroendocrine tumors (NETs), to identify patients who should be referred for o

276 eptor (SSTR)-positive neuroendocrine tumors (NETs).

277 ring in patients with neuroendocrine tumors (NETs).

278 poorly differentiated neuroendocrine tumors (NETs).

279 nteropancreatic (GEP) neuroendocrine tumors (NETs).

280 F-mFBG PET data showed correlation to tumour NET-1 protein expression, while further studies are need

281 -2 (SSTR2)-expressing neuroendocrine tumour (NET) though tumour regression occurs in only a minority

282 s typically used for neuroendocrine tumours (NETs).

283 Methods: Twenty-two NET patients underwent a 45-min dynamic PET/CT scan afte

284 ermittent haemodialysis suggest that fast UF(NET) rates are also associated with ischaemic injury to

285 In addition, fast UF(NET) rates are associated with an increased risk of card

286 are required to examine whether moderate UF(NET) rates are associated with a reduced risk of haemody

287 ncreased mortality compared with moderate UF(NET) rates.

288 The UF(NET) rate should be prescribed based on patient body wei

289 id removal (that is, net ultrafiltration (UF(NET))) during continuous kidney replacement therapy are

290 d it constitutes the basis for understanding NETs-mediated immune and hemostatic responses.

291 g atherosclerotic plaques and stenosis using NETs may lay a groundwork for future clinical detection

292 d activation may neutralize pathogens, vital NET formation, and prolonged neutrophil viability, and i

293 ther studies are needed to elucidate whether NET-1 upregulation induced by blocking mTOR might be a u

294 ote tumor growth and metastases, but whether NETs impact the tumor immune microenvironment remains un

295 However, whether NETs infiltrate particular compartments in severe COVID-

296 flammatory diseases, we investigated whether NETs would be involved in COVID-19 pathophysiology.

297 nflammatory areas of the interstitium, while NET-prone primed neutrophils were present in arteriolar

298 vivo was performed, and data correlated with NET-1 protein levels measured ex vivo.

299 a therapy monitoring tool for patients with NETs.

300 D28-mediated Th17 induction, with or without NETs.