ライフサイエンスコーパス: MPO

1 MPO and affected pathways represent attractive targets f

2 MPO is a glycoprotein (GP) chaperoned by calreticulin (C

3 MPO is a homodimeric glycoprotein, posttranslationally m

4 MPO is an abundant neutrophil-derived heme protein that

5 MPO mutations contribute significantly to GPP's pathogen

6 MPO mutations, primarily those resulting in complete MPO

7 MPO potentially can be heavily modified as it harbors 5

8 MPO protein and activity measurements and histologic ana

9 MPO screening in conditions phenotypically related to GP

10 MPO was primarily secreted by neutrophils, followed by l

11 MPO+ ANCA EGPA is an eosinophilic autoimmune disease sha

12 MPO-Sp but not OVA-Sp administration increased MPO-speci

13 MPO-specific CD4(+) effector T cell proliferation was en

14 omogeneous assays could detect 5.2 mug L(-1) MPO (35 pM) via a faster cycle.

15 MMPs (1, 2, 3, 7, 8, 9, 12), MPO, and tissue inhibitor of matrix metalloproteinase (T

16 infections had been documented in 2/6 (33%) MPO-deficient patients.

17 mutations in the NADPH oxidase complex or a MPO-deficient patient were examined.

18 R3-positive AAV (PR3-AAV), MPO-positive AAV (MPO-AAV) and, for EGPA, by the presence or absence of AN

19 er classified as PR3-positive AAV (PR3-AAV), MPO-positive AAV (MPO-AAV) and, for EGPA, by the presenc

20 Lysosomal-accumulated MPO can be both cell-protective, by promoting the degrad

21 ades after the first description of acquired MPO deficiency in MPN, we provide the molecular correlat

22 We hypothesized that acquired MPO deficiency in MPN could be associated with the prese

23 We describe (18)F-MAPP, an activatable MPO activity radioprobe for positron emission tomography

24 l cholesterol, and myeloperoxidase activity (MPO) were measured.

25 We then administered MPO- and OVA-conjugated apoptotic splenocytes (MPO-Sps a

26 tent of endotoxin-induced inflammation in an MPO-dependent manner.

27 ly, treatment of healthy neutrophils with an MPO inhibitor (4-Aminobenzoic acid hydrazide) increased

28 Saliva MMP-8, MMP-9, TIMP-1, and MPO concentrations distinguished periodontitis patients

29 f smoking, whereas saliva MMP-9, TIMP-1, and MPO were mostly affected by time since cessation, especi

30 ted with LMZ [1.15 (95% CI: 1.01, 1.31)] and MPO [1.16 (1.01, 1.34)].

31 Serum MMP-9 and MPO levels were higher in women with PCOS and gingivitis

32 NE, MMP-8, MMP-9, and MPO levels were elevated in oGVHD tears when compared wi

33 In controls, NE, MMP-9, and MPO significantly correlated with each other (P < .0001)

34 ted strongly with elevated MMP-8, MMP-9, and MPO suggests a common neutrophilic source and provides e

35 were performed between NE, MMP-8, MMP-9, and MPO within study groups.

36 It induces anti-MPO T-cell autoimmunity and MPO-ANCA in mice, whereas related sequences do not.

37 Moreover, CD162 and MPO expression increased significantly in intermediate m

38 Likewise, increased CD162 and MPO expression was noted in CD14(++)CD16(-) classical mo

39 tform for electrical detection of h-FABP and MPO in physiological saline.

40 Deploying FABP and MPO specific scFvs as receptor molecules onto our high-s

41 label-free screening of heart type-FABP and MPO.

42 ckdown experiments, silencing GP-5, GRN, and MPO decreased PLTs.

43 of MPO activity, competitive inhibition, and MPO deficiency in living animals, confirming specificity

44 uced tissue injury and implicate PMN-MPs and MPO as important regulators of cellular function.

45 Anti-MPO antibody transfer resulted in nephritic urine by dip

46 of specially engineered anti-h-FABP and anti-MPO single-chain fragment variables (scFv) were immobili

47 MPO409-428 as a therapeutic attenuated anti-MPO GN.

48 ated by autoimmunity to MPO (autoimmune anti-MPO GN), we assessed the capacity for nasal tolerance in

49 erized mice to animals with established anti-MPO autoimmunity attenuated the subsequent development o

50 Mice with established anti-MPO autoimmunity that received CD4(+) T cells transferre

51 In mice with established anti-MPO autoimmunity, nasal insufflation of MPO409-428 as a

52 A-Sp to recipient mice with established anti-MPO autoimmunity.

53 reated with OVA-Sp) were protected from anti-MPO autoimmunity and GN, confirming the induction of the

54 -Sp administration did not protect from anti-MPO autoimmunity or GN.

55 cell epitope (MPO(409-428)), can induce anti-MPO autoimmunity.

56 We induced anti-MPO GN by immunizing mice with MPO and a low dose of ant

57 The peptide induces anti-MPO autoreactivity in the context of three MHC class II

58 It induces anti-MPO T-cell autoimmunity and MPO-ANCA in mice, whereas re

59 of disease attenuated injury in murine anti-MPO GN.

60 tis and mice with anti-myeloperoxidase (anti-MPO) antibody-induced NCGN.

61 Studies in experimental models of anti-MPO GN suggest that, after ANCA-induced neutrophil local

62 effects on development and severity of anti-MPO GN.

63 We used passive anti-MPO antibody transfer for NCGN induction in wild-type mi

64 ) type 1 regulatory T cells and reduced anti-MPO autoimmunity and GN.

65 e immunodominant MPO peptide suppresses anti-MPO GN by inducing antigen-specific tolerance.

66 reased in serum, but not in urine, with anti-MPO antibody treatment and was completely abolished with

67 e and NGAL-deficient chimeric mice with anti-MPO antibody-induced NCGN.

68 C = 0.86) currently employed MPO approaches (MPO, AUC = 0.61; MPO_V2, AUC = 0.67).

69 , IL-6 downward arrow, HMGB1 downward arrow, MPO downward arrow, CD68 downward arrow, IL-4 upward arr

70 aminepentaacetate gadolinium, referred to as MPO-Gd, and cross-linked iron oxide nanoparticle (CLIO-N

71 T1-weighted MRI was used to assess MPO activity, and T2*-weighted MRI was used to track CLI

72 The enzymatic activity of PMN-MP-associated MPO was enhanced compared with soluble protein, leading

73 0] vs 1.02 [95% CI: 0.89, 1.14]; P = .03) at MPO-Gd MR imaging.

74 s self-calibrating carbon nanomaterial-based MPO activity indicators.

75 However, the causal relationship between MPO and the development and progression of atheroscleros

76 cell clones exacerbated disease mediated by MPO-specific CD4(+) cells in Rag1(-/-) mice.

77 creases with the progression of oxidation by MPO/H(2)O(2)/Cl(-) due to the formation of graphene quan

78 (b) catalase-like cycle was slower, and (c) MPO retained enzymatically active conformation after com

79 er, we identified a pathogenic CD8(+) T cell MPO epitope (MPO431-439) and found that cotransfer of MP

80 sculitis and the nephritogenic murine T cell MPO epitope emphasizes the clinical relevance of this st

81 ver, in mice depleted of regulatory T cells, MPO-Sp administration did not protect from anti-MPO auto

82 MS approaches, we structurally characterized MPO from neutrophils of healthy human donors.

83 se of the deleterious effects of circulating MPO, there is a great interest in the development of new

84 of the CNS MPO scoring algorithm, termed CNS MPO.v2.

85 indings led to a modified version of the CNS MPO scoring algorithm, termed CNS MPO.v2.

86 tors, and favorable druglike properties (CNS-MPO, Fsp(3), LELP).

87 tions, primarily those resulting in complete MPO deficiency, cumulatively associated with GPP (p = 1.

88 Conclusion MPO is a suitable imaging biomarker for identifying and

89 Conclusion MPO-Gd showed elevated MPO activity in NAFLD mouse model

90 Complex carbohydrates decorate MPO at discrete sites, but their functional relevance re

91 Decreased MPO activity was substantiated by the absence of 3-chlor

92 However, lysosomal-delivered MPO also disrupts lysosomal acidification in RPE cells,

93 xtracellular space, with lysosomal-delivered MPO exhibiting a half-life of 10 h.

94 ransiently recruits neutrophils that deposit MPO in glomeruli.

95 A-induced neutrophil localization, deposited MPO within glomeruli is recognized by autoreactive T cel

96 ls, strongly implicating bone-marrow-derived MPO in the pathogenesis of CKD atherosclerosis.

97 xperiments confirmed that neutrophil-derived MPO contributes importantly to protection from endotoxem

98 myeloperoxidase (MPO) activity, could detect MPO activity in nonalcoholic steatohepatitis (NASH) mous

99 e for over half a year to reliably determine MPO.

100 unprocessed proMPO versus the mature dimeric MPO and the functional role of the propeptide.

101 presents intrinsic neutrophil proteins (eg, MPO [myeloperoxidase] and various proteinases) but can g

102 We discovered eight MPO mutations resulting in MPO -deficiency in neutrophil

103 18)F-MAPP imaging detected sites of elevated MPO activity in living mice embedded with human MPO and

104 Conclusion MPO-Gd showed elevated MPO activity in NAFLD mouse models and human liver biops

105 outperformed (AUC = 0.86) currently employed MPO approaches (MPO, AUC = 0.61; MPO_V2, AUC = 0.67).

106 ency of Ly6G+/4HN+ neutrophils; and enhanced MPO activity.

107 ous to an immunodominant MPO T-cell epitope (MPO(409-428)), can induce anti-MPO autoimmunity.

108 n antibacterial activity including BPI, EPX, MPO and AZU1.

109 Although considered important for MPO structure and function, the full scope and relative

110 GE binding protein and between CS and NS for MPO.

111 These results show a pathogenic role for MPO-specific CD8(+) T cells, provide evidence that CD8(+

112 ated, and transplanted with bone marrow from MPO-deficient mice to induce bone marrow MPO deletion (C

113 ing chemotherapy treatment, elicited further MPO-dependent increase in TOP2A and especially TOP2B-DNA

114 rwent MRI at 9.4 T and received gadodiamide, MPO-Gd, or CLIO-NPs.

115 To generate MPO-specific regulatory T cells, we used a modified prot

116 While similar global MPO glycosylation was observed across conditions, the co

117 vival rate and decreased the levels of H2O2, MPO, NO, TNFalpha, IL-6 and IL-10 in compressed muscle.

118 High MPO-expressing AML cells were less sensitive to AraC in

119 ining oxidative stress, particularly in high MPO-expressing AML cells.

120 However, MPO was associated with a lower risk of high transferrin

121 of SPIN bound to a recombinant form of human MPO at 2.4-A resolution.

122 strong homology between the pathogenic human MPO B cell epitope recognized by ANCA in patients with a

123 activity in living mice embedded with human MPO and in mice induced with chemical inflammation or my

124 These findings identify MPO as a genetic determinant of pustular skin disease an

125 of potential applications of GO for imaging MPO activity in live cells.

126 ty, we transplanted irradiated MPO-immunized MPO-deficient mice with bone marrow from either wild-typ

127 e also transplanted irradiated MPO-immunized MPO/IL-17A double-deficient mice with bone marrow from e

128 eus peptide, homologous to an immunodominant MPO T-cell epitope (MPO(409-428)), can induce anti-MPO a

129 diimide (ECDI), to couple the immunodominant MPO peptide (MPO(409-428)) or a control ovalbumin peptid

130 lenocytes conjugated with the immunodominant MPO peptide suppresses anti-MPO GN by inducing antigen-s

131 We implicate MPO as an inflammatory modulator in humans that regulate

132 imaged with gadopentetate dimeglumine and in MPO knockout NASH mice with MPO-Gd, which proves specifi

133 ells (p = 0.015), and phagocytosis assays in MPO-deficient mice and human cells revealed altered neut

134 zygous splice-site mutation (c.2031-2A>C) in MPO.

135 enhance the regulatory role of mast cells in MPO-AAV.

136 nd IL-6 (P = .0001) that mirrored changes in MPO activity.

137 s supporting a posttranscriptional defect in MPO production.

138 GPP and demonstrated effects of mutations in MPO encoding the neutrophilic enzyme myeloperoxidase (MP

139 The enhancement was reduced in MPO knockout mice (mean signal intensity ratio at 60 min

140 discovered eight MPO mutations resulting in MPO -deficiency in neutrophils and monocytes.

141 Although several steps in MPO biosynthesis and processing have been elucidated, ma

142 O-Sp but not OVA-Sp administration increased MPO-specific, peripherally derived CD4(+)Foxp3(-) type 1

143 ctants (MIP-2, KC), neutrophil infiltration (MPO activity), lipid peroxidation (4-HNE), and nitric ox

144 ctional findings provide novel insights into MPO biosynthesis and processing.

145 T(H)17 immunity, we transplanted irradiated MPO-immunized MPO-deficient mice with bone marrow from e

146 icient mice; we also transplanted irradiated MPO-immunized MPO/IL-17A double-deficient mice with bone

147 sm-based inhibitor and inhibits irreversibly MPO at nanomolar concentration.

148 ion (MPO/SCN(-)/H(2)O(2)) and catalase-like (MPO/H(2)O(2)) cycles.

149 al oxygen consumption when compared with low MPO-expressing AML cells.

150 aracterized by increased CD3(+) lymphocytes, MPO(+) cells and elevated TNF-alpha and IL-17 mRNA level

151 ECT/CT imaging of MPO activity showed marked MPO-sensor retention at 6 hours (P = .003) that continue

152 rom MPO-deficient mice to induce bone marrow MPO deletion (CKD-bMPOKO) or bone marrow from WT mice as

153 a control to maintain preserved bone marrow MPO(CKD-bMPOWT).

154 vage to the heavy and light chains of mature MPO protomers, and (iii) three covalent bonds between he

155 scribe electrochemical approaches to measure MPO by using the pseudohalogenation (MPO/SCN(-)/H(2)O(2)

156 In patients with increased DNA methylation, MPO and PRTN3 expression correlated with DNA methylation

157 nce of ischemic lesions associated with mild MPO-mediated enhancement in the thoracolumbar spine at 2

158 slational candidate to noninvasively monitor MPO activity and inflammation in patients.

159 PMN-MP/MPO-dependent inhibition of IEC wound healing was due to

160 The number of mutant MPO alleles significantly differed between 82 affected i

161 ce markers (CD106, CD162 and myeloperoxidase MPO) was analyzed.

162 Myeloperoxidase (MPO) concentration in stool, used as a quantitative inde

163 Myeloperoxidase (MPO) is a critical proinflammatory enzyme implicated in

164 Myeloperoxidase (MPO) is a well defined autoantigen in ANCA-associated va

165 Myeloperoxidase (MPO) is synthesized by neutrophil and monocyte precursor

166 Myeloperoxidase (MPO) plays essential roles in neutrophil-mediated immuni

167 Myeloperoxidase (MPO), a key enzyme released by neutrophils during inflam

168 Myeloperoxidase (MPO)-ANCA-associated GN is a significant cause of renal

169 metalloproteinase (MMP)-9, myeloperoxidase (MPO), neutrophil elastase (NE), and MMP-9/tissue inhibit

170 he pathogenesis of acquired myeloperoxidase (MPO) deficiency, a rare phenomenon observed in patients

171 irected to proteinase 3 and myeloperoxidase (MPO) in particular are associated with distinct forms of

172 alloproteinases (MMPs), and myeloperoxidase (MPO) in tear washes of patients with ocular graft-vs-hos

173 male wild-type (n = 23) and myeloperoxidase (MPO) knock-out (n = 5) mice were infected with the Plasm

174 alloproteinase (TIMP)-1 and myeloperoxidase (MPO).

175 vatives would abrogate anti-myeloperoxidase (MPO) antibody-induced NCGN in a mouse model.

176 n oxidation product (APOP), myeloperoxidase (MPO) and nitric oxide (NO), while depleting levels of en

177 e action of enzymes such as myeloperoxidase (MPO) or NADPH oxidase, and the release of neutrophil ext

178 mmation and permeability by myeloperoxidase (MPO), neopterin (NEO), and alpha-1-antitrypsin (AAT) con

179 phil markers, Calprotectin, Myeloperoxidase (MPO), and IL-8 are significantly increased at time of di

180 to detect and characterize myeloperoxidase (MPO) are needed, given that this "split personality" enz

181 The heme enzyme myeloperoxidase (MPO) participates in innate immune defense mechanism thr

182 ing the neutrophilic enzyme myeloperoxidase (MPO).

183 oxygen species, the enzymes myeloperoxidase (MPO) and neutrophil elastase.

184 imaging agent specific for myeloperoxidase (MPO) activity, could detect MPO activity in nonalcoholic

185 ibodies (ANCA) specific for myeloperoxidase (MPO).

186 on of the autoantigen genes myeloperoxidase (MPO) and proteinase 3 (PRTN3) in leukocytes of patients

187 ly binds and inhibits human myeloperoxidase (MPO), a major player in the oxidative defense of neutrop

188 s were immunised with human myeloperoxidase (MPO).

189 Increased myeloperoxidase (MPO) expression and activity are associated with atheros

190 in, the inflammatory marker myeloperoxidase (MPO), and the cytokine receptor for nuclear factor kappa

191 ions in experimental murine myeloperoxidase (MPO)-ANCA-associated vasculitis (AAV) show mast cells de

192 Neutrophil myeloperoxidase (MPO) catalyzes the H2O2-dependent oxidation of chloride

193 decreasing the activity of myeloperoxidase (MPO) and the expression of pro-inflammatory mediators.

194 eroxide and the presence of myeloperoxidase (MPO) derived from inflammatory cells, which are active p

195 kade or genetic deletion of myeloperoxidase (MPO), a key neutrophil enzyme, significantly increased m

196 nosorbent assay analysis of myeloperoxidase (MPO), tumor necrosis factor (TNF)-alpha, interleukin (IL

197 proteinase 3 (PR3-ANCA) or myeloperoxidase (MPO-ANCA).

198 ne (AraC) and overexpressed myeloperoxidase (MPO), a heme protein that converts hydrogen peroxide to

199 (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal

200 We measured plasma myeloperoxidase (MPO)-DNA complexes (NETs), platelet factor 4, RANTES, an

201 Specifically, myeloperoxidase (MPO), which is abundantly expressed in PMN azurophilic g

202 ging technologies targeting myeloperoxidase (MPO) can reveal early inflammation associated with spina

203 pensable constituent of the myeloperoxidase (MPO)-H2 O2 -halide system that produces the potent micro

204 flammatory response through myeloperoxidase (MPO) and biologically promoting metastasis during inflam

205 Autoreactivity to myeloperoxidase (MPO) causes anti-neutrophil cytoplasmic antibody (ANCA)-

206 t options for patients with myeloperoxidase (MPO)-ANCA-associated GN are needed.

207 etween groups of EC and NS (myeloperoxidase [MPO], matrix metalloproteinase-9) as well as between DS

208 inding proteins (FABP) and myeloperoxidases (MPO) are associated with many chronic conditions in huma

209 fflation of the immunodominant nephritogenic MPO peptide (MPO409-428) to attenuate this disease.

210 ynthesis-activity relationship of neutrophil MPO (nMPO).

211 utations had reduced MPO protein, but normal MPO messenger RNA (mRNA) levels supporting a posttranscr

212 cytometric analyses characterized CLIO-NPs, MPO, endothelial cells, and leukocytes.

213 Zileuton (a leukotriene inhibitor) to obtain MPO and neutrophil targeting NPs, denoted as HZ-5 NPs.

214 The absence of MPO expression in the bone marrow and atherosclerotic le

215 chronic cellular uptake and accumulation of MPO in lysosomes coincides with N-retinylidene-N-retinyl

216 osure results in progressive accumulation of MPO in lysosomes.

217 ers delays germination through the action of MPO and NADPH oxidase, and restricts fungal growth throu

218 correlated with higher enzyme activities of MPO in distinct granule populations.

219 at (a) SCN(-) did not affect the affinity of MPO for H(2)O(2), (b) catalase-like cycle was slower, an

220 invasively differentiated varying amounts of MPO activity, competitive inhibition, and MPO deficiency

221 possible implications for the application of MPO inhibitors in cardiovascular diseases.

222 terogeneous immunoassays with the capture of MPO on d/Ab could detect 60 mug L(-1), which was suitabl

223 cellular uptake and lysosomal degradation of MPO mediates elimination of this harmful enzyme, whereas

224 rosclerosis in CKD mice with the deletion of MPO in bone marrow cells, strongly implicating bone-marr

225 tor-mediated cellular uptake and delivery of MPO to lysosomes of retinal pigmented epithelial (RPE) c

226 h was suitable for the accurate detection of MPO in human saliva (101% recovery).

227 en the recent interest in the development of MPO antagonists for the treatment of neurodegenerative d

228 is study uncovers a noncanonical function of MPO enzyme in maintaining redox balance and mitochondria

229 tive disease demonstrated hypomethylation of MPO and PRTN3 and increased expression of the autoantige

230 SPECT/CT imaging of MPO activity showed marked MPO-sensor retention at 6 hou

231 en administered before or after induction of MPO autoimmunity in these mice, disodium cromoglycate at

232 To gain insight into inhibition of MPO by SPIN, we solved the cocrystal structure of SPIN b

233 ere performed after intravenous injection of MPO sensors (bis-5-hydroxytryptamide-tetraazacyclododeca

234 f 3-chlorotyrosine, a specific by-product of MPO, in aortic atherosclerotic lesions as determined by

235 ammatory diseases leads to redistribution of MPO to the extracellular space, where it can mediate tis

236 pproach, we report novel functional roles of MPO glycans, providing new insight into neutrophil-media

237 inds to proteins and accumulates at sites of MPO activity.

238 ice with MPO-Gd, which proves specificity of MPO-Gd.

239 A retrospective cohort study of MPO- or PR3-ANCA-positive patients with AAV (MPA and GPA

240 termination of enzymes; for example, time of MPO quantification was cut from 3-4 h (sandwich ELISA) t

241 the atypical glycosylation pattern found on MPO might contribute to its specific processing and pres

242 elected by this virtual method and tested on MPO in vitro.

243 GBI, PD, MPO, ABL, and histopathologic examinations demonstrated

244 ), to couple the immunodominant MPO peptide (MPO(409-428)) or a control ovalbumin peptide (OVA(323-33

245 ch were transgenic for a myeloid peroxidase (MPO)-specific TCR.

246 Plasma MPO-DNA complexes increased in COVID-19, with intubation

247 ess severity correlated directly with plasma MPO-DNA complexes (P = .0360), whereas Pao2/fraction of

248 at S. aureus secretes a unique proteinaceous MPO inhibitor to enhance survival by interfering with MP

249 e genes (MMP8, OLFM4, LCN2/NGAL, LTF, PRTN3, MPO) and also of 5 genes involved in the immunological s

250 measure MPO by using the pseudohalogenation (MPO/SCN(-)/H(2)O(2)) and catalase-like (MPO/H(2)O(2)) cy

251 for advanced glycation end products [RAGE], MPO, uteroglobin/CC-10); between groups of DS and NS for

252 impaired leukocyte extravasation and reduced MPO activity in lungs.

253 s with homozygous CALR mutations had reduced MPO protein, but normal MPO messenger RNA (mRNA) levels

254 on in plasma by the physiologically relevant MPO-H(2)O(2)-NO(2) (-) system.

255 Results MPO-Gd enhancement occurred in inflammatory CM hotspots

256 arameters and serum MMP-9 levels or salivary MPO, NE levels, and MMP-9/MMP-1 ratio.

257 O- and OVA-conjugated apoptotic splenocytes (MPO-Sps and OVA-Sps, respectively) to mice and compared

258 From a therapeutic standpoint, MPO catalyzes the in vitro degradation of N-retinylidene

259 Lysosomal-targeted MPO exerts both cell-protective and cytotoxic functions.

260 Targeting MPO expression or enzyme activity sensitized AML cells t

261 d tomography (CT) (n = 15) studies targeting MPO activity were performed after intravenous injection

262 However, evidence has emerged that MPO-derived oxidants contribute to propagation of inflam

263 The MPO targeting property of 5-HT modified NPs is confirmed

264 neutrophil chemoattractants, as well as the MPO activity in the lungs of septic mice.

265 d the Asn323-/Asn483-glycans, located in the MPO dimerisation zone, was found to affect the local gly

266 r-truncated Asn355-glycans positioned in the MPO-ceruloplasmin interface are critical for uninterrupt

267 we perform photoluminescence studies on the MPO-catalyzed oxidation of graphene oxide (GO) and surfa

268 g that prevents H2O2 substrate access to the MPO active site.

269 suggest that a molecular hotspot within the MPO molecule contains important CD8(+), CD4(+), and B ce

270 tudy, 20 leptin receptor-deficient and three MPO knockout mice were injected with endotoxin (lipopoly

271 elative abundance of the glycans attached to MPO is unknown.

272 l necrotizing GN mediated by autoimmunity to MPO (autoimmune anti-MPO GN), we assessed the capacity f

273 We induced autoimmunity to MPO by immunizing mice with MPO in adjuvant; to trigger

274 Our sensors show linear response to MPO oxidative machinery and hold the promise to be used

275 vivo studies showed that nasal tolerance to MPO is mediated by both conventional and induced T regul

276 We also show that proMPO-to-MPO maturation occurs during early/mid-stage granulopoie

277 nflammation have raised interest in tracking MPO activity in patients.

278 Eleven human liver biopsy samples underwent MPO-Gd-enhanced MR imaging ex vivo and subsequent histol

279 e radioprobe can quantify changes in in vivo MPO activity.

280 GD(391-410), develop glomerulonephritis when MPO is deposited in glomeruli.

281 CD4(+) cells mediated glomerular injury when MPO was planted in glomeruli.

282 eases inside the neutrophil phagosome, where MPO is located, compared with outside the neutrophil.

283 apoptosis, highlighting a mechanism whereby MPO mutations affect granulocyte numbers.

284 Purpose To test whether MPO-Gd, an activatable molecular magnetic resonance (MR)

285 on molecule) were associated with PLT, while MPO (myeloperoxidase) showed significant association wit

286 It remains unclear why MPO is frequently the target of antibody-mediated autoim

287 ical features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGP

288 ich relapse was induced by re-challenge with MPO.

289 N in IL-17A-deficient chimeras compared with MPO-deficient mice receiving wild-type bone marrow, as w

290 enzymes of IL-36 precursors, correlated with MPO deficiency.

291 erimental NASH and underwent MR imaging with MPO-Gd.

292 itor to enhance survival by interfering with MPO-mediated killing.

293 induced anti-MPO GN by immunizing mice with MPO and a low dose of anti-glomerular basement membrane

294 autoimmunity to MPO by immunizing mice with MPO in adjuvant; to trigger GN, we used low-dose antiglo

295 meglumine and in MPO knockout NASH mice with MPO-Gd, which proves specificity of MPO-Gd.

296 Five out of 6 patients with MPO deficiency carried a homozygous CALR mutation and we

297 by staining the single cell suspensions with MPO and CitH3 Abs.

298 ) T cells transferred from mice treated with MPO-Sp (but not CD4(+) T cells transferred from mice tre

299 erring CD4(+) T cells from mice treated with MPO-Sp or OVA-Sp to recipient mice with established anti

300 GAL-deficient bone marrow developed worsened MPO-ANCA-induced NCGN.