ライフサイエンスコーパス: ANCA

1 ANCA activate primed neutrophils (and monocytes) by bind

2 ANCA activates neutrophils and activated neutrophils dam

3 ANCA and B cell levels lacked sufficient sensitivity to

4 ANCA disease remains a subject of great experimental and

5 ANCA negativity was associated with a decreased proporti

6 ANCA negativity was associated with an increased proport

7 ANCA rises correlated with relapses in patients who pres

8 ANCA specificity independently predicts relapse among pa

9 ANCA specificity was predictive of relapse, with PR3 ANC

10 ANCA-activated neutrophils activate the alternative comp

11 ANCA-activated neutrophils not only induce injury but lo

12 ANCA-activated phagocytes cause vasculitis and necrotizi

13 ANCA-associated vasculitides are characterized by inflam

14 ANCA-associated vasculitis (AAV) is a highly inflammator

15 ANCA-associated vasculitis can be induced in various for

16 ANCA-associated vasculitis is an autoimmune condition ch

17 ANCA-associated vasculitis is the most frequent cause of

18 ANCA-induced phagocyte NADPH oxidase (Phox) may contribu

19 ANCA-induced superoxide and IL-1beta generation were inv

20 ANCAs activate neutrophils inducing their respiratory bu

21 an increase in ANCA levels, except for the 1 ANCA-negative patient.

22 -SD) follow-up of 49+/-33 months and 18+/-14 ANCA measurements, 89 ANCA rises and 74 relapses were re

23 Nine centers enrolled 197 ANCA-positive patients with either Wegener's granulomato

24 Anti-proteinase 3 ANCA was associated with HLA-DP and the genes encoding a

25 less frequently than those with proteinase 3 ANCA, suggesting greater immune regulation.

26 ry support for the concept that proteinase 3 ANCA-associated vasculitis and myeloperoxidase ANCA-asso

27 a central pathogenic feature of proteinase 3 ANCA-associated vasculitis.

28 g African Americans, those with proteinase 3-ANCA (PR3-ANCA) had 73.3-fold higher odds of having HLA-

29 ated from patients and chimeric proteinase 3-ANCA induced the release of neutrophil microparticles fr

30 e with myeloperoxidase-ANCA and proteinase 3-ANCA.

31 -33 months and 18+/-14 ANCA measurements, 89 ANCA rises and 74 relapses were recorded.

32 Antineutrophil cytoplasmic Abs (ANCAs) specific for myeloperoxidase (MPO) play a role in

33 elial growth factor, in patients with active ANCA-associated vasculitis compared with patients during

34 ltured neutrophils from patients with active ANCA-associated vasculitis, indicating that increased tr

35 ipheral granulocytes of patients with active ANCA-associated vasculitis.

36 -MPO antibodies, increase sFlt1 during acute ANCA-associated vasculitis, leading to an antiangiogenic

37 Serum from patients with acute ANCA-associated vasculitis disrupted blood flow in the c

38 al models of anti-MPO GN suggest that, after ANCA-induced neutrophil localization, deposited MPO with

39 Although ANCA levels fell after rituximab therapy, relapse was no

40 HR 1.89 [95% CI 1.33-2.69], P = 0.0004), and ANCA specificity had the best predictive model fit (mode

41 ationship between anti-LAMP-2 antibodies and ANCA glomerulonephritis.

42 F-alpha, beta2-integrin engagement, C5a, and ANCA by the FcgammaRII receptor.

43 ith conventional markers of inflammation and ANCA titers.

44 uch as IgA nephropathy, lupus nephritis, and ANCA GN; and additional features as detailed herein.

45 t had antineutrophil cytoplasmic antibodies (ANCA) against proteinase 3 (PR3).

46 Antineutrophil cytoplasmic antibodies (ANCA) are positive in ~40% of the cases and more often i

47 Antineutrophil cytoplasmic antibodies (ANCA) are present in many patients, vary in level over t

48 dhood antineutrophil cytoplasmic antibodies (ANCA) associated vasculitides and to identify the import

49 genic antineutrophil cytoplasmic antibodies (ANCAs) can result in systemic small vessel vasculitis.

50 f how antineutrophil cytoplasmic antibodies (ANCAs) contribute to the pathophysiology of vasculitis.

51 e of anti-neutrophil cytoplasmic antibodies (ANCAs) directed against proteinase 3 (PR3).

52 ce of antineutrophil cytoplasmic antibodies (ANCAs) in the phenotypic expression of Churg-Strauss syn

53 hich anti-neutrophil cytoplasmic antibodies (ANCAs) may contribute to the pathogenesis of ANCA-associ

54 Antineutrophil cytoplasmic antibodies (ANCAs) target proteins normally retained within neutroph

55 pical antineutrophil cytoplasmic antibodies (ANCAs) was performed separately using commercially avail

56 ed by antineutrophil cytoplasmic antibodies (ANCAs), but most patients with neuropathy lack ANCAs.

57 clinical antineutrophil cytoplasm antibody (ANCA) associated vasculitis.

58 ntial of anti-neutrophil cytoplasm antibody (ANCA) has provided a rationale for antibody removal by P

59 d in the anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitides (AAV).

60 ents with antineutrophil cytoplasm antibody (ANCA)-associated vasculitides.

61 with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis.

62 ecause anti-neutrophil cytoplasmic antibody (ANCA) and anti-PR3 antibody screening can be negative at

63 xpress anti-neutrophil cytoplasmic antibody (ANCA) antigens, and activation of these cells by ANCA is

64 e (MPO) antineutrophil cytoplasmic antibody (ANCA) experience relapses less frequently than those wit

65 c and antineutrophilic cytoplasmic antibody (ANCA) testing.

66 del of anti-neutrophil cytoplasmic antibody (ANCA) vasculitis.

67 sis of anti-neutrophil cytoplasmic antibody (ANCA)-associated necrotizing crescentic GN (NCGN) is inc

68 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) may be localized or

69 ies for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are limited by partial

70 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) constitutes life-threa

71 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a common cause of r

72 seases, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), a chronic, severe dis

73 ens for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis are effective in 70 to 90% o

74 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis exhibits endothelial damage,

75 severe antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis for 40 years.

76 ractory antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis in small studies.

77 Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a severe condition encomp

78 -2) in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is controversial because of

79 tening) antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is unknown.

80 free in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and a pair of urinary prote

81 However, 10%-15% of patients are ANCA negative and the cause of their injury is unknown.

82 mimicking a small vessel vasculitis such as ANCA-associated GN, are a very rare manifestation of den

83 -neutrophil cytoplasmic antibody-associated (ANCA-associated) small vessel necrotizing vasculitis is

84 ociated with gene silencing are perturbed at ANCA autoantigen-encoding genes, potentially contributin

85 t antineutrophil cytoplasmic autoantibodies (ANCA) are pathogenic.

86 f antineutrophil cytoplasmic autoantibodies (ANCA) in addition to the more commonly known targets pro

87 r antineutrophil cytoplasmic autoantibodies (ANCA).

88 Antineutrophil cytoplasmic autoantibody (ANCA) causes vascular injury that leads to small-vessel

89 Anti-neutrophil cytoplasmic autoantibody (ANCA) disease rarely occurs in African Americans and ris

90 Antineutrophil cytoplasmic autoantibody (ANCA) vasculitis is a systemic autoimmune disease result

91 asthma and sinusitis, distinguishing between ANCA-negative CSS and PDGFR-negative HES is difficult be

92 ry, we identified a mechanistic link between ANCA-induced neutrophil activation, necroptosis, NETs, t

93 ught to investigate the relationship between ANCA status and the clinical expression of CSS in a case

94 fibrosis, noncystic fibrosis bronchiectasis, ANCA-associated vasculitis and bronchiectasis.

95 e NF-kappaB in primed human neutrophils, but ANCA-stimulated primed neutrophils activated NF-kappaB i

96 By ANCA specificity, categories of GPA, MPA, and kidney-lim

97 ) antigens, and activation of these cells by ANCA is central to ANCA-associated vasculitis and necrot

98 anulomatous inflammation may be initiated by ANCA-induced activation of extravascular neutrophils, ca

99 trials, we advocate classifying patients by ANCA serotype as opposed to the traditional disease type

100 genic human MPO B cell epitope recognized by ANCA in patients with acute vasculitis and the nephritog

101 were evident when analysis was stratified by ANCA type, AAV diagnosis (granulomatosis with polyangiit

102 and was not influenced by disease category, ANCA subtype, or remission duration before KTX.

103 dult-derived treatment regimens in childhood ANCA-associated vasculitides.

104 ding of the clinical phenotypes of childhood ANCA-associated vasculitides and improved our ability to

105 The most common ANCA target antigens are myeloperoxidase (MPO) and prote

106 eta-galactosidase or neuraminidase converted ANCA assay results from negative to positive.

107 ic cytokine in patients with newly diagnosed ANCA-associated crescentic GN.

108 3:1 ratio, 44 patients with newly diagnosed ANCA-associated vasculitis and renal involvement to a st

109 8(+) T cells mediate disease in experimental ANCA-associated vasculitis.

110 linical manifestations, histologic findings, ANCA staining patterns, and the presence of antibodies t

111 Rituximab is effective for ANCA-associated and cryoglobulinemic vasculitis with neu

112 is of patients enrolled in the Rituximab for ANCA-Associated Vasculitis (RAVE) Trial who had renal in

113 ine the efficacy and safety of rituximab for ANCA-associated vasculitis in a larger multicenter cohor

114 histopathological classification system for ANCA-associated vasculitis was recently published, but w

115 rocesses may provide therapeutic targets for ANCA-mediated diseases in humans.

116 ardiolipin, and tested strongly positive for ANCAs in a perinuclear pattern by immunofluorescence.

117 NCA-positive patients, these antibodies from ANCA-negative patients failed to bind the more complexly

118 , in contrast to anti-LAMP-2 antibodies from ANCA-positive patients, these antibodies from ANCA-negat

119 NETs from ANCA-stimulated neutrophils caused endothelial cell (EC)

120 ned the PR3 and MPO loci in neutrophils from ANCA patients and healthy control individuals for epigen

121 ls were higher in patients who suffered from ANCA-associated renal relapses compared with those in pa

122 tokine-producing anti-MPO T cells and higher ANCA titers than control mice.

123 ce also led to more anti-MPO T cells, higher ANCA titers, and more severe GN after immunization with

124 IgA ANCA were found in approximately 30% of patients and wer

125 FcR genotypes, IgA ANCA, and IgG ANCA are potential prognostic and therapeu

126 cR genetics and previously unappreciated IgA ANCA affect clinical presentation.

127 FcR genotypes, IgA ANCA, and IgG ANCA are potential prognostic and therapeutic targets fo

128 fluorescence assays to determine IgA and IgG ANCA positivity, and used Illumina, TaqMan, or Pyroseque

129 When stimulated with IgA and IgG ANCA together, IgG ANCA induced neutrophil activation wa

130 Neutrophil stimulation by IgA or IgG ANCA led to degranulation and neutrophil extracellcular

131 imulated with IgA and IgG ANCA together, IgG ANCA induced neutrophil activation was reduced (P = 0.00

132 e-associated membrane protein-2 (hLAMP-2) in ANCA-associated piFNGN, and have now investigated whethe

133 hodology led to the discovery of MPO-ANCA in ANCA-negative disease that reacted against a sole linear

134 idase (MPO) is a well defined autoantigen in ANCA-associated vasculitis.

135 ibitor of metalloproteinase-1, and CXCL13 in ANCA-associated vasculitis.

136 rial of Rituximab versus Cyclophosphamide in ANCA-Associated Vasculitis trial.

137 NETs have been consistently detected in ANCA-associated small-vessel vasculitis, and this associ

138 y sought to determine whether differences in ANCA epitope specificity explain why, in some cases, con

139 ibodies and their relationship to disease in ANCA glomerulonephritis are not well described.

140 Management of eye disease in ANCA-associated vasculitis includes local anti-inflammat

141 or H3K27me3, was preferentially expressed in ANCA patients versus healthy controls.

142 Given roles for FcRs in ANCA-mediated neutrophil activation and IgA antibodies i

143 m the development of focal necrotizing GN in ANCA-associated vasculitis.

144 re accompanied or preceded by an increase in ANCA levels, except for the 1 ANCA-negative patient.

145 encing, were depleted at PR3 and MPO loci in ANCA patients compared with healthy controls.

146 o inappropriate expression of PR3 and MPO in ANCA patients.

147 pecificities different from those present in ANCA disease.

148 ation was increased at the RUNX3 promoter in ANCA patients.

149 er for disease activity and renal relapse in ANCA-associated crescentic GN.

150 o cyclophosphamide for inducing remission in ANCA-associated vasculitis.

151 associated with ANCA positivity or a rise in ANCA levels.

152 Participants in the Rituximab in ANCA-Associated Vasculitis (RAVE) trial were excluded fr

153 V: 163 subjects enrolled in the Rituximab in ANCA-Associated Vasculitis trial were screened for the p

154 ntigen gene expression and disease status in ANCA-associated vasculitis, we measured gene-specific DN

155 hat CD8(+) cells are a therapeutic target in ANCA-associated vasculitis, and suggest that a molecular

156 ith cyclophosphamide as induction therapy in ANCA-associated vasculitis.

157 now investigated whether the same is true in ANCA-negative patients.

158 CSS with sufficient documentation, including ANCA status.

159 tion and diagnostic systems that incorporate ANCA specificity, such as PR3 ANCA-positive MPA and MPO

160 with and activated by NET components induce ANCA and autoimmunity when injected into naive mice.

161 CAs), but most patients with neuropathy lack ANCAs.

162 , microscopic polyangiitis, or renal-limited ANCA-associated vasculitis in complete remission after a

163 copic polyangiitis, and 5 with renal-limited ANCA-associated vasculitis) received azathioprine (58 pa

164 eping the inflammasome in check and limiting ANCA-induced inflammation.

165 In conclusion, longitudinal ANCA measurements may be useful in patients with renal i

166 The value of measuring ANCA during follow-up to predict a relapse is controvers

167 logic insights, we postulated that measuring ANCA is useful in patients with renal involvement but is

168 icity, such as PR3 ANCA-positive MPA and MPO ANCA-positive MPA, provide a more useful tool than the c

169 CA with specificity for myeloperoxidase (MPO ANCA) versus ANCA with specificity for proteinase 3 (PR3

170 twice as likely to relapse as those with MPO ANCA (HR 1.89 [95% CI 1.33-2.69], P = 0.0004), and ANCA

171 Rodent models of both myeloperoxidase (MPO) ANCA and proteinase 3 (PR3) ANCA associated vasculitis h

172 einase 3 (PR3)-ANCA or myeloperoxidase (MPO)-ANCA, were included in our study, followed at regular in

173 ions for patients with myeloperoxidase (MPO)-ANCA-associated GN are needed.

174 in experimental murine myeloperoxidase (MPO)-ANCA-associated vasculitis (AAV) show mast cells degranu

175 r intervals, and tested for PR3-ANCA and MPO-ANCA.

176 of myeloperoxidase-specific antibodies (MPO-ANCA).

177 in-vivo work in this field has concerned MPO-ANCA associated disease, although the last year has seen

178 The role of genetics in MPO-ANCA NCGN severity was investigated using 13 inbred mous

179 effector responses can induce injury in MPO-ANCA-associated microscopic polyangiitis.

180 as induced either by passive transfer of MPO-ANCA and LPS or by planting MPO(409-428) conjugated to a

181 this methodology led to the discovery of MPO-ANCA in ANCA-negative disease that reacted against a sol

182 There is evidence that MPO-ANCA cause necrotizing and crescentic glomerulonephritis

183 l involvement (72 with PR3-ANCA, 32 with MPO-ANCA) and 62 patients had nonrenal disease (36 with PR3-

184 renal disease (36 with PR3-ANCA, 26 with MPO-ANCA).

185 CA-associated vasculitis and myeloperoxidase ANCA-associated vasculitis are distinct autoimmune syndr

186 Anti-myeloperoxidase ANCA was associated with HLA-DQ (P=2.1x10(-8)).

187 eutrophil myeloperoxidase in myeloperoxidase-ANCA-associated microscopic poliangiitis providing a pot

188 s similar in both those with myeloperoxidase-ANCA and proteinase 3-ANCA.

189 A new ANCA, directed against human lysosome membrane protein-2

190 anti-LAMP-2 reactivity was present in 21% of ANCA sera from two of the centers; reactivity was presen

191 eroxidase (MPO) underlies the development of ANCA-associated vasculitis and GN, but the mechanisms un

192 Therefore, we studied the effect of ANCA on NF-kappaB activation in neutrophil/EC cocultures

193 The two salient features of ANCA-associated vasculitis (AAV) are the restricted micr

194 The various forms of ANCA disease share some characteristics, and similar the

195 hil cytoplasmic antibodies are a hallmark of ANCA-associated vasculitides and are likely to be integr

196 r understanding of the immunopathogenesis of ANCA-associated vasculitides.

197 elapse-free period (P<0.001), independent of ANCA serotype.

198 Bony erosion was independent of ANCA status or systemic involvement.

199 uing immunosuppression, and investigation of ANCA and B cell levels as re-treatment biomarkers.

200 ents with biopsy-proven renal involvement of ANCA-associated vasculitis.

201 ouse MPO (anti-MPO) induces a mouse model of ANCA NCGN that closely mimics human disease.

202 ate the underlying cause and pathogenesis of ANCA vasculitis.

203 important insights into the pathogenesis of ANCA-associated pulmonary and renal disease.

204 ANCAs) may contribute to the pathogenesis of ANCA-associated vasculitis are not well understood.

205 This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, show

206 rophil microparticles in the pathogenesis of ANCA-associated vasculitis, potentially providing a targ

207 ctivation is involved in the pathogenesis of ANCA-associated vasculitis.

208 immunodominant epitopes in the pathology of ANCA-associated vasculitis and suggest that autoantibody

209 tions were with the antigenic specificity of ANCA, not with the clinical syndrome.

210 myeloid dendritic cells and the induction of ANCAs and associated autoimmunity.

211 results in the induction and persistence of ANCAs is not well understood.

212 GPA and MPA; and 3) classification based on ANCA with specificity for myeloperoxidase (MPO ANCA) ver

213 of inflammatory bowel disease had elevated p-ANCA antibody levels compared to 3 of 15 controls (20%)

214 g bowel disease, and one-half had elevated p-ANCA levels.

215 ear antineutrophil cytoplasmic antibodies (p-ANCAs) with specificities for 'atypical' antigens.

216 In this study, both polyclonal ANCAs isolated from patients and chimeric proteinase 3-A

217 Finally, IgG from LAMP-2-positive ANCA-negative patients bound specifically to normal huma

218 ADAM17 in active proteinase-3 (PR3)-positive ANCA-associated vasculitis (AAV).

219 re were 38 (40.9%) of 93 cases with positive ANCA results, of which 15 cases reported a positive ELIS

220 ANCA with specificity for proteinase 3 (PR3 ANCA).

221 ualized based on serial B lymphocyte and PR3 ANCA monitoring.

222 at incorporate ANCA specificity, such as PR3 ANCA-positive MPA and MPO ANCA-positive MPA, provide a m

223 cificity was predictive of relapse, with PR3 ANCA-positive patients almost twice as likely to relapse

224 Concomitant injection of anti-PR3 ANCAs with PR3-expressing apoptotic cells induced a Th17

225 peroxidase (MPO) ANCA and proteinase 3 (PR3) ANCA associated vasculitis have been developed, which ha

226 itis, positive for either proteinase 3 (PR3)-ANCA or myeloperoxidase (MPO)-ANCA, were included in our

227 Americans, those with proteinase 3-ANCA (PR3-ANCA) had 73.3-fold higher odds of having HLA-DRB1*15 al

228 sociation between the DRB1*15 allele and PR3-ANCA disease, among African Americans.

229 The differences between PR3-ANCA-associated vasculitis (AAV) and MPO-AAV described i

230 teinase-3 (PR3) mAb and serum containing PR3-ANCA from patients with active vasculitis both induced a

231 wed at regular intervals, and tested for PR3-ANCA and MPO-ANCA.

232 lleles contribute to the pathogenesis of PR3-ANCA disease.

233 However, the serum containing polyclonal PR3-ANCA did not induce release of sFlt1 from cultured human

234 Among Caucasians, those with PR3-ANCA had 2.2-fold higher odds of carrying DRB1*1501 than

235 2 patients had nonrenal disease (36 with PR3-ANCA, 26 with MPO-ANCA).

236 patients had renal involvement (72 with PR3-ANCA, 32 with MPO-ANCA) and 62 patients had nonrenal dis

237 ence of cocaine in any patient with presumed ANCA vasculitis, and if positive, then urine should also

238 patients receiving rituximab for refractory ANCA-associated vasculitis at 4 centers in the UK was us

239 e remission induction therapy for refractory ANCA-associated vasculitis in this study.

240 of 80 to 90% among patients with refractory ANCA-associated vasculitis and may be safer than cycloph

241 r necrosis and crescent formation in a renal ANCA-associated vasculitis model.

242 s were higher in sera of patients with renal ANCA disease compared with those in sera of patients wit

243 n a prospective study of patients with renal ANCA disease.

244 uspicion should be maintained, with repeated ANCA testing, biopsy, and imaging where indicated, espec

245 it is a single disease entity and what role ANCA plays in its pathogenesis.

246 dard intravenous cyclophosphamide for severe ANCA-associated vasculitis.

247 rine (AZA) for remission-induction in severe ANCA-associated vasculitis (AAV), but renal outcomes are

248 eatment for induction of remission in severe ANCA-associated vasculitis and may be superior in relaps

249 In patients with severe ANCA-associated vasculitis, a single course of rituximab

250 Still, ANCA pathogenesis remains obscure.

251 ovide insight into how PR3 and PR3-targeting ANCAs promote GPA pathophysiology.

252 asingly clear over the last two decades that ANCA IgG is pathogenic in vasculitis.

253 Here we report that ANCA induces neutrophil extracellular traps (NETs) via r

254 We suggest that ANCA-stimulated neutrophils activate endothelial NF-kapp

255 tion with clinical trials has confirmed that ANCAs directly contribute to the evolution and progressi

256 The ANCA-associated GN (AGN) classification categorizes pati

257 The ANCA-associated vasculitides, granulomatosis with polyan

258 disease, and that in limited eye disease the ANCA is frequently undetected.

259 xpressed a variety of markers, including the ANCA autoantigens proteinase 3 and myeloperoxidase.

260 The genesis of the ANCA autoimmune response is a multifactorial process tha

261 el localization of the disease is due to the ANCA antigen accessibility, which is restricted to the m

262 ivation of these cells by ANCA is central to ANCA-associated vasculitis and necrotizing crescentic gl

263 re, we detected LAMP-2 autoantibodies in two ANCA-negative patients.

264 In patients with GN or vasculitis, ANCAs are directed against proteinase 3 (PR3) or myelope

265 ficity for myeloperoxidase (MPO ANCA) versus ANCA with specificity for proteinase 3 (PR3 ANCA).

266 ivation in neutrophil/EC cocultures in vitro ANCA did not activate NF-kappaB in primed human neutroph

267 At the time of KTX, 29 patients were ANCA-positive.

268 d be closely considered in any patient where ANCA vasculitis is entertained given the wide use of the

269 is a highly inflammatory condition in which ANCA-activated neutrophils interact with the endothelium

270 n exist in disease-free individuals, and why ANCA are undetected in patients with ANCA-negative disea

271 mab therapy, relapse was not associated with ANCA positivity or a rise in ANCA levels.

272 scopic polyangiitis that are associated with ANCA specificity, and suggests that the response against

273 ly discuss all drug culprits associated with ANCA vasculitis and then focus on clinical, serologic, t

274 r immunoglobulin deposits is associated with ANCA.

275 -complex (MHC) and non-MHC associations with ANCA-associated vasculitis and also that granulomatosis

276 icroparticles in the plasma of children with ANCA-associated vasculitis compared with that in healthy

277 Patients with ANCA aberrantly express neutrophil granule-encoding gene

278 NCGN severity varies among patients with ANCA disease, and genetic factors influence disease seve

279 ry low titers in a minority of patients with ANCA disease.

280 es (two academic centers) from patients with ANCA glomerulonephritis (n=329); those with ANCA-negativ

281 m for PR3 and MPO disrupted in patients with ANCA vasculitis, we examined the PR3 and MPO loci in neu

282 upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of cres

283 are enriched in the kidneys of patients with ANCA-associated crescentic GN and colocalize with CXCR3(

284 upregulated in the kidneys of patients with ANCA-associated crescentic GN as opposed to patients wit

285 s of renal biopsy samples from patients with ANCA-associated crescentic GN.

286 More patients with ANCA-associated vasculitides had sustained remission at

287 ral to disease pathogenesis in patients with ANCA-associated vasculitis (AAV).

288 discovery cohort of 1233 U.K. patients with ANCA-associated vasculitis and 5884 controls and was rep

289 ht have therapeutic benefit in patients with ANCA-associated vasculitis and GN.

290 tudinal analysis revealed that patients with ANCA-associated vasculitis could be divided into two gro

291 ctively, among three groups of patients with ANCA-associated vasculitis from Vienna, Austria (n=19);

292 ase 3 (PRTN3) in leukocytes of patients with ANCA-associated vasculitis observed longitudinally (n=82

293 Observations in patients with ANCA-associated vasculitis suggest that CD8(+) T cells p

294 cheme with which to categorize patients with ANCA-associated vasculitis, but adding the percentage of

295 hundred sixty-six consecutive patients with ANCA-associated vasculitis, positive for either proteina

296 n be detected in most European patients with ANCA-associated vasculitis.

297 and why ANCA are undetected in patients with ANCA-negative disease.

298 In conclusion, in patients with ANCA-negative piFNGN, we have identified autoantibodies

299 ANCA glomerulonephritis (n=329); those with ANCA-negative glomerulonephritis (n=104); those with fim

300 utoantigens in patients with vasculitis with ANCA.

301 izing GN (piFNGN) is usually associated with ANCAs that are thought to be pathogenic.