ライフサイエンスコーパス: JIA

1 JIA patients had a naive T cell compartment with shorten

2 JIA-associated uveitis carries significant ocular morbid

3 ught for 21 SNPs in a second cohort of 1,015 JIA cases and 1,569 controls collected in the US and Ger

4 We identified 8,479 JIA patients with 13,003 person-years of followup; 36% t

5 Gene expression data on 68 JIA cases and 23 local controls showed cis expression qu

6 The initial cohort included 809 JIA cases and 3,535 controls of non-Hispanic, European a

7 study of 103 consecutive adults attending a JIA continuity clinic, and patients who consented comple

8 mumab after withdrawal of the IMP for active JIA-U (median time to flare 188 days [range 42-413 days)

9 ipants were started on adalimumab for active JIA-U.

10 cents 2 years of age or older who had active JIA-associated uveitis.

11 o among children and adolescents with active JIA-associated uveitis who were taking a stable dose of

12 ents in the canakinumab group had an adapted JIA ACR 30 response (36 of 43 [84%], vs. 4 of 41 [10%] i

13 The primary outcome, termed adapted JIA ACR 30 response, was defined as improvement of 30% o

14 corrected for age was abnormally high in all JIA subtypes (enthesitis-related arthritis was not asses

15 Among JIA patients not receiving TNF inhibitor therapy, MTX us

16 significant for T1D (0.863+/-s.e. 0.07) and JIA (0.727+/-s.e. 0.037), more modest for UC (0.386+/-s.

17 at the diseases UC-CD (0.69+/-s.e. 0.07) and JIA-CVID (0.343+/-s.e. 0.13) are the most strongly corre

18 to evaluate the association between CMA and JIA and to test whether exposure to antibiotics would be

19 C strongly contribute to SNP-h(2) in T1D and JIA, but does not significantly contribute to the pairwi

20 lescents with juvenile idiopathic arthritis (JIA) and pediatric inflammatory bowel disease (pIBD).

21 patients with juvenile idiopathic arthritis (JIA) are matters of concern, especially in patients trea

22 es, including juvenile idiopathic arthritis (JIA) has earned substantial attention in the last 10 yea

23 chronicity of juvenile idiopathic arthritis (JIA) into adulthood and attendant potential disability m

24 ria parse out juvenile idiopathic arthritis (JIA) into seven groups, with the aim of creating homogen

25 Juvenile idiopathic arthritis (JIA) is a heterogeneous group of inflammatory diseases,

26 Juvenile idiopathic arthritis (JIA) is a wide group of diseases, characterized by synov

27 Systemic juvenile idiopathic arthritis (JIA) is an autoinflammatory syndrome in which the myelom

28 ssociation in juvenile idiopathic arthritis (JIA) is complicated by age-dependent IgG glycan variatio

29 Juvenile Idiopathic Arthritis (JIA) is one of the most common chronic disease condition

30 Systemic juvenile idiopathic arthritis (JIA) is the most severe subtype of JIA; treatment option

31 thogenesis of juvenile idiopathic arthritis (JIA) is thought to involve multiple components of the ce

32 icipants with juvenile idiopathic arthritis (JIA) or suspected of having JIA (seven boys, 38 girls; m

33 icipants with juvenile idiopathic arthritis (JIA) or suspected of having JIA and showed agreement wit

34 In juvenile idiopathic arthritis (JIA) patients, we have previously reported that atypical

35 patients with juvenile idiopathic arthritis (JIA) to determine the predictors of MTXGlu variability i

36 children with juvenile idiopathic arthritis (JIA) typically rely on parents as proxy respondents.

37 for detecting juvenile idiopathic arthritis (JIA) was developed based on the immobilization of the PR

38 ic feature of juvenile idiopathic arthritis (JIA), but the relevance of these unusual cells to this d

39 ividuals with juvenile idiopathic arthritis (JIA), comprising the most common subtypes (oligoarticula

40 n subtypes of juvenile idiopathic arthritis (JIA), IgM rheumatoid factor-negative polyarticular JIA a

41 ng autoimmune juvenile idiopathic arthritis (JIA), result from a complex interplay between genetics a

42 In juvenile idiopathic arthritis (JIA), there are now more than 25 regions represented by

43 cular form of juvenile idiopathic arthritis (JIA), using 2 independent cohorts to ascertain the seque

44 patients with juvenile idiopathic arthritis (JIA), we have previously described findings limited to a

45 patients with juvenile idiopathic arthritis (JIA)-associated uveitis treated with topical corticoster

46 pertaining to juvenile idiopathic arthritis (JIA)-associated uveitis.

47 s of systemic juvenile idiopathic arthritis (JIA).

48 seases called juvenile idiopathic arthritis (JIA).

49 children with juvenile idiopathic arthritis (JIA).

50 ggregation of juvenile idiopathic arthritis (JIA).

51 patients with juvenile idiopathic arthritis (JIA).

52 children with juvenile idiopathic arthritis (JIA).

53 rgy (CMA) and juvenile idiopathic arthritis (JIA).

54 treatment of juvenile idiopathic arthritis (JIA).

55 patients with juvenile idiopathic arthritis (JIA).

56 e immunity in juvenile idiopathic arthritis (JIA).

57 iagnoses with juvenile idiopathic arthritis (JIA; adjusted hazard ratio [aHR], 0.38; 95% confidence i

58 poly-articular and extended oligo-articular JIA patients, before and after anti-TNF therapy withdraw

59 We have demonstrated associations between JIA and variants in the TNFAIP3, STAT4, and C12orf30 reg

60 ities overall as well as differences between JIA subtypes.

61 nd may explain disease heterogeneity between JIA subtypes and between autoimmune diseases in general.

62 ducational achievement was not influenced by JIA subtype (F = 1.18, P = 0.33).

63 dings limited to autoimmunity loci shared by JIA and other diseases.

64 nced by functional disability rather than by JIA subtype.

65 The discovery cohort consisted of Caucasian JIA cases (n = 814) and local controls (n = 658) genotyp

66 Here, we review current JIA association findings and the recent progress in the

67 ignificantly robust genetic associations for JIA.

68 at least three of the six core criteria for JIA, worsening of more than 30% in no more than one of t

69 The PAR of familial factors for JIA was approximately 13%.

70 e spectroscopy showed RCT 3 times higher for JIA positive sample than for a pool of human serum sampl

71 me to identify novel susceptibility loci for JIA.

72 n College of Rheumatology [ACR] core set for JIA, with no more than one variable worsening by more th

73 The treatment for JIA, including TNF inhibitors, did not appear to be sign

74 prevented by addition of synovial fluid from JIA patients, through an IL-6-independent mechanism.

75 nd protein are found in synovial fluids from JIA patients.

76 detected in spontaneously forming NETs from JIA patient synovial neutrophils, and DEK-targeted aptam

77 dren with CMA; 66 of these children also had JIA.

78 athic arthritis (JIA) or suspected of having JIA (seven boys, 38 girls; median age, 14 years [interqu

79 athic arthritis (JIA) or suspected of having JIA and showed agreement with contrast-enhanced MRI.

80 (LD) blocks containing previously identified JIA-associated SNPs demonstrated higher regulation poten

81 to assess the efficacy of biologic agents in JIA-associated uveitis.

82 ssed proteins may be potential biomarkers in JIA.

83 method for screening biomarker candidates in JIA.

84 gamma9(+)Vdelta2(+) (Vgamma9(+)) T cells, in JIA.

85 /rare variants remain to be characterised in JIA, and represent a possible example of synthetic assoc

86 may be an important parameter to consider in JIA classification.

87 Inherited HLA factors in JIA show similarities overall as well as differences bet

88 tributable risk (PAR) of familial factors in JIA.

89 As we identified DEK in synovial fluids in JIA patients, we now investigate how DEK protein and/or

90 inflammation may reduce risk of hypotony in JIA-associated uveitis.

91 contribute directly to joint inflammation in JIA by generating ICs through high-affinity interaction

92 contribute directly to joint inflammation in JIA by generating immune complexes through high affinity

93 is locally produced in an inflamed joint in JIA.

94 is locally produced in an inflamed joint in JIA.

95 is, plasma BLyS protein levels are normal in JIA despite elevated blood leukocyte BLyS mRNA levels.

96 ajority of proteins showed overexpression in JIA synovial fluid as compared with noninflammatory cont

97 including the interleukin (IL)-2 pathway, in JIA disease pathogenesis.

98 sed on preliminary criteria for remission in JIA.

99 ciations between MTXGlu and drug response in JIA.

100 lationships between CD4(+) T cell subsets in JIA, using high-throughput TCR repertoire analysis.

101 munity are shared across diseases, including JIA, suggesting the potential for common therapeutic tar

102 bility of paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributab

103 ough anti-TNF therapy has strongly increased JIA remission rates, it is not curative and up to 80% of

104 We confirmed association of 3 known JIA risk loci (the human leukocyte antigen (HLA) region,

105 Using a large JIA cohort, we sought to identify additional clusters of

106 rther analyses elucidated significantly more JIA SNPs with regulatory potential compared to 1KGP data

107 sequels, there is an imperative need for new JIA diagnosis strategies.

108 We also identified a non-JIA comparator cohort of children diagnosed as having at

109 esent study was undertaken to identify novel JIA-predisposing loci using genome-wide approaches.

110 We also demonstrated enrichment of novel JIA variants in histone modification peaks and DNase hyp

111 Approximately 13% of cases of JIA can be attributed to familial factors.

112 file in children with selected categories of JIA.

113 The category of JIA, sex, and age at diagnosis were not associated with

114 he role of genetic variation in the cause of JIA will provide insight for disease mechanism and may e

115 we sought to identify additional clusters of JIA cases and to calculate robust estimates of the relat

116 n summary, this is the largest collection of JIA cases investigated so far and provides new insight i

117 k (RR) of JIA in the siblings and cousins of JIA probands.

118 ere associated with the later development of JIA (odds ratio = 2.4, 95% confidence interval: 1.6, 3.6

119 ibiotic exposure in the later development of JIA.

120 d from children with a definite diagnosis of JIA (n = 98).

121 ould start immediately when the diagnosis of JIA is suspected or confirmed and be continued for more

122 and the length of time from the diagnosis of JIA to the initiation of anti-TNFalpha therapy, the dura

123 for more than 8 years after the diagnosis of JIA.

124 gene expression findings provide evidence of JIA association at 3q13 and suggest novel genes as plaus

125 phages were purified from synovial fluids of JIA patients.

126 association approach to the investigation of JIA.

127 tion was able to amass sufficient numbers of JIA and control samples to identify significantly robust

128 h a diagnosis of uveitis before the onset of JIA all developed cataract and had an OR for development

129 Short duration between the onset of JIA and the diagnosis of uveitis was a risk factor for d

130 Patients with onset of JIA between January 1997 and June 2000 were prospectivel

131 leukocyte antigen (HLA-)B27, age of onset of JIA, and sex were analyzed for their predictive value fo

132 bodies may contribute to the pathogenesis of JIA.

133 bodies may contribute to the pathogenesis of JIA.

134 ull) CD8+ T cells, in the pathophysiology of JIA.

135 n in children, including the predilection of JIA for early childhood, remains to be defined.

136 Drug-induced remission of JIA-U did not persist when adalimumab was withdrawn afte

137 in an estimated 18, 13 and 6% of the risk of JIA, respectively.

138 probands with JIA have an increased risk of JIA.

139 mmunity and integrity in boys with a risk of JIA.

140 The RR of JIA in first cousins was also increased (5.82, 95% CI 2.

141 The RR of JIA in the siblings of patients was significantly increa

142 obust estimates of the relative risk (RR) of JIA in the siblings and cousins of JIA probands.

143 We have identified the largest sets of JIA pedigrees described to date.

144 otein expression according to the subtype of JIA.

145 rthritis (JIA) is the most severe subtype of JIA; treatment options are limited.

146 ase from patients with different subtypes of JIA and in healthy controls, providing evidence of immun

147 erentially expressed between the subtypes of JIA and is locally produced in an inflamed joint in JIA.

148 oints in patients with different subtypes of JIA, there are differences in protein expression accordi

149 ression differs in the different subtypes of JIA.

150 ld change; P < 0.05) between the subtypes of JIA.

151 tion accounts for approximately one-third of JIA susceptibility.

152 K aptamers hold promise for the treatment of JIA and other types of arthritis.

153 ogic agents hold promise in the treatment of JIA-associated uveitis, but require long-term data to as

154 e efficacy of adalimumab in the treatment of JIA-associated uveitis.

155 processes may lead to improved treatment of JIA.

156 egative polyarticular JIA and oligoarticular JIA.

157 patients with extended-to-be oligoarticular JIA (0.57 compared with 0.90 in the persistent disease g

158 IA and 9 with active extended oligoarticular JIA was assessed by real-time polymerase chain reaction

159 is is most common in extended oligoarticular JIA.

160 o in contrast to findings for oligoarticular JIA, patients with polyarticular arthritis had no eviden

161 was a significant feature of oligoarticular JIA (n = 62) as compared to polyarticular JIA (n = 36).

162 he likelihood of extension of oligoarticular JIA to a more severe disease phenotype.

163 nts with early- or late-onset oligoarticular JIA (with 97% accuracy) or from patients with early- or

164 Patients with recent-onset oligoarticular JIA were identified and grouped according to those whose

165 ic JIA (sJIA), 187 persistent oligoarticular JIA (pOJIA), and 139 extended OJIA (eOJIA) patients], an

166 onset JIA (39 with persistent oligoarticular JIA, 45 with rheumatoid factor-negative polyarticular JI

167 (P = 0.03) and in those with oligoarticular JIA (t = 2.29, P = 0.02).

168 similar between patients with oligoarticular JIA and a younger subgroup of patients with polyarticula

169 of samples from patients with oligoarticular JIA and patients with polyarticular JIA.

170 1104, found in the group with oligoarticular JIA and the group of younger patients with polyarticular

171 ) in PBMCs from children with oligoarticular JIA whose disease began before age 6 years (early-onset

172 s obtained from children with oligoarticular JIA, polyarticular JIA, or systemic JIA were compared.

173 s between patients with early-and late-onset JIA, independent of classification based on the number o

174 controls and 104 patients with recent-onset JIA (39 with persistent oligoarticular JIA, 45 with rheu

175 on diagnosis codes for MAS and either SLE or JIA.

176 e, sex, and race distribution of the overall JIA cohort.

177 Compared with ADHD patients, JIA patients who were not currently taking MTX or TNF in

178 a focus on early childhood, the time of peak JIA incidence.

179 early-onset oligoarticular and polyarticular JIA patients, including female preponderance, antinuclea

180 ldren with oligoarticular JIA, polyarticular JIA, or systemic JIA were compared.

181 IgM rheumatoid factor-negative polyarticular JIA and oligoarticular JIA.

182 and rheumatoid factor-negative polyarticular JIA), and 13,056 controls.

183 ith rheumatoid factor-negative polyarticular JIA, and 20 with systemic JIA).

184 ents with early- or late-onset polyarticular JIA (with 89% accuracy), but not from patients with syst

185 of children with recent-onset polyarticular JIA resulted in clinical inactive disease by 6 months an

186 ar JIA (n = 62) as compared to polyarticular JIA (n = 36).

187 children ages 2-16 years with polyarticular JIA of <12 months' duration.

188 Furthermore, patients with polyarticular JIA showed age-specific related effects, with disease su

189 group of younger patients with polyarticular JIA.

190 rticular JIA and patients with polyarticular JIA.

191 nger subgroup of patients with polyarticular JIA.

192 ver, prior studies have shown that psoriatic JIA (psJIA) may be a heterogeneous entity.

193 1 and DRB1*0701 were protective for selected JIA subtypes.

194 n Caucasian paediatric cohorts [219 systemic JIA (sJIA), 187 persistent oligoarticular JIA (pOJIA), a

195 , 2 to 17 years of age, with active systemic JIA (duration of >/=6 months and inadequate responses to

196 tissue from 12 patients with active systemic JIA and 9 with active extended oligoarticular JIA was as

197 synovium was constrained in active systemic JIA compared to the known IFN-mediated extended oligoart

198 Monocytes in patients with active systemic JIA retain the ability to respond to IFNgamma, suggestin

199 ta) therapy, 5 patients with active systemic JIA, and 8 healthy controls were incubated with or witho

200 N- induced gene signature in active systemic JIA.

201 Anakinra as first-line therapy for systemic JIA was associated with rapid resolution of systemic sym

202 in monocytes tended to be higher in systemic JIA patients compared to healthy controls, with the high

203 show the efficacy of canakinumab in systemic JIA with active systemic features.

204 s not assessed), most strikingly in systemic JIA.

205 leukin-6 plays a pathogenic role in systemic JIA.

206 ine, rather than rescue, therapy in systemic JIA.

207 in STAT1 in patients with inactive systemic JIA compared to controls, and a greater increase in IRF1

208 cytes from 3 patients with inactive systemic JIA receiving anti-interleukin-1beta (anti-IL-1beta) the

209 In patients with inactive systemic JIA who received treatment with anti-IL-1beta, hyperresp

210 nocytes from patients with inactive systemic JIA.

211 rimary outcome was time to flare of systemic JIA.

212 594 patients with polyarticular or systemic JIA treated with etanercept only, etanercept plus methot

213 rticular JIA, polyarticular JIA, or systemic JIA were compared.

214 s efficacious in severe, persistent systemic JIA.

215 atients, 2 to 19 years of age, with systemic JIA and active systemic features (fever; >/=2 active joi

216 curacy), but not from patients with systemic JIA or healthy controls.

217 Patients with systemic JIA receiving anakinra as part of initial disease-modify

218 tive polyarticular JIA, and 20 with systemic JIA).

219 pheral monocytes from patients with systemic JIA.

220 k between siblings and cousins suggests that JIA is influenced by shared genetic factors.

221 The JIA cohort included 7,812 children with a total followup

222 The JIA cohort included 8,503 children with 13,990 person-ye

223 This biosensor was able to discriminate the JIA positive and negative serum samples from different i

224 gle outcome, there were 42 infections in the JIA cohort (incidence rate 300 per 100,000 person-years;

225 o the age, sex, and race distribution of the JIA cohort.

226 r of genetic variants that may contribute to JIA and give us some clues into what may trigger this di

227 ologies necessary to apply this knowledge to JIA association findings.

228 dence suggests that the microbiota's link to JIA begins in early childhood, as early life events that

229 Predisposing factors related to JIA pathogenesis seem to display a sex-linked disparity.

230 icipants stopped adalimumab for uncontrolled JIA-U.

231 ill likely provide a basis for understanding JIA genetic risk.

232 ch communities particularly in understanding JIA etiology.

233 th uveitis, and 4 of 80 patients (5.0%) with JIA-U had binocular decreased VA <6/12.

234 unocompromised children and adolescents with JIA and pIBD receiving TNF-alpha inhibitors.

235 ease variables for employment in adults with JIA.

236 nically effective in uveitis associated with JIA; however, its cost effectiveness is not demonstrated

237 owed suggestive evidence of association with JIA (P < 1 x 10(-6)).

238 e initial cohort suggested associations with JIA in 13 distinct loci.

239 The strongest associations with JIA risk or protection were observed for TNFAIP3 variant

240 identified several further associations with JIA subtypes.

241 005, we identified a cohort of children with JIA and a comparator cohort of children with attention d

242 ypes of infections reported in children with JIA and pIBD treated with TNF-alpha inhibitors.

243 s the first deep WGS effort on children with JIA and provides useful genetic resources for research c

244 2005, we identified cohorts of children with JIA and without JIA according to the diagnosis codes use

245 Children with JIA appeared to have an increased rate of incident malig

246 to predict disease outcome in children with JIA are currently available.

247 005, we identified a cohort of children with JIA based on physician diagnosis codes and dispensed med

248 Nevertheless, children with JIA had a higher rate of opportunistic infections, inclu

249 Children with JIA had an increased rate of infection compared to child

250 ycophenolate mofetil, and more children with JIA received interleukin-1 antagonists.

251 For all children with JIA versus children without JIA, the SIR was 4.4 (95% co

252 opportunistic infections among children with JIA were 3 cases of Coccidioides (incidence rate 21 per

253 Among children with JIA who had undergone primary immunization, MMR booster

254 Among children with JIA, the rate of infection was not increased with MTX or

255 Compared to children with JIA, those with SLE had a similar mortality rate (6% ver

256 lteration of the microbiota in children with JIA.

257 en with underlying SLE than in children with JIA.

258 g 19 children with SLE and 102 children with JIA.

259 estoration of normal growth in children with JIA.

260 stic infections are rare among children with JIA.

261 rmalities of the microbiota in children with JIA; mechanisms by which an altered microbiota at birth

262 atomic force microscopy, after contact with JIA positive serum, presented great globular clusters ir

263 who had significantly more descendants with JIA than expected (5-13 descendants; P values ranged fro

264 and between 2000 and 2010 and diagnosed with JIA (n = 1,298) and age-, sex-, and place-matched contro

265 most evident in boys who were diagnosed with JIA before age 3 years or diagnosed with CMA with predom

266 terior uveitis cases included diagnosis with JIA, Behcet's disease, bilateral uveitis, history of cat

267 In patients with JIA (n = 141), the G0:G1 ratio was elevated compared wit

268 quivalence trial including 137 patients with JIA aged 4 to 9 years who were recruited from 5 academic

269 loci was accomplished for 820 patients with JIA and 273 control subjects.

270 ol for determining outcomes in patients with JIA being treated with MTX.

271 One-third of patients with JIA can successfully undergo withdrawal of treatment wit

272 Patients with JIA from a single center (n = 99; mean +/- SD age 117.8

273 ve chart review in a cohort of patients with JIA treated with TNFalpha inhibitors between January 1,

274 fying antirheumatic drug-naive patients with JIA were characterized using high-performance liquid chr

275 ood samples were obtained from patients with JIA who were being treated with a stable dose of MTX for

276 er cross-sectional analysis of patients with JIA who were receiving stable doses of MTX at a tertiary

277 by matching the records of 862 patients with JIA with the records of approximately 7 million individu

278 sent was obtained from the 104 patients with JIA, blood was withdrawn during routine MTX-screening la

279 In this cohort of patients with JIA, the MTXGlu(TOT) concentration varied 40-fold.

280 in the synovial fluid (SF) of patients with JIA, this study was undertaken to investigate how DEK pr

281 ot been previously reported in patients with JIA, were detected.

282 lycans in healthy children and patients with JIA, with a focus on early childhood, the time of peak J

283 All patients with JIA-associated uveitis (N = 108; affected eyes = 196) ev

284 but significant proportion of patients with JIA-associated uveitis and is associated with signs of a

285 s in improving the outcomes of patients with JIA-related uveitis.

286 is deviation is exaggerated in patients with JIA.

287 t outcomes in a group of adult patients with JIA.

288 rotein were found in the SF of patients with JIA.

289 s were purified from the SF of patients with JIA.

290 developed in 96 (22.1%) of 434 patients with JIA.

291 r the occurrence of uveitis in patients with JIA.

292 nal subsets of CD8+ T cells in patients with JIA.

293 to aid decision making by young people with JIA.

294 Siblings and first cousins of probands with JIA have an increased risk of JIA.

295 Children with SLE and those with JIA received cyclosporine at similar rates, but more chi

296 More patients with SLE than those with JIA received ICU care (63% versus 27%; P = 0.002), recei

297 ied cohorts of children with JIA and without JIA according to the diagnosis codes used by their physi

298 ll children with JIA versus children without JIA, the SIR was 4.4 (95% confidence interval [95% CI] 1

299 dent malignancy compared to children without JIA.

300 ared with no booster did not result in worse JIA disease activity and was immunogenic.