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

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

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

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

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

13 286) were also available from North American JIA cases (n=747) and controls (n=1,161).

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

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

16 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

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

18 s were analyzed for association with JIA and JIA subtypes.

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

20 management of juvenile idiopathic arthritis (JIA) along with activity level, functional abilities and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 s of systemic juvenile idiopathic arthritis (JIA).

45 seases called juvenile idiopathic arthritis (JIA).

46 children with juvenile idiopathic arthritis (JIA).

47 ggregation of juvenile idiopathic arthritis (JIA).

48 patients with juvenile idiopathic arthritis (JIA).

49 treatment of juvenile idiopathic arthritis (JIA).

50 children with juvenile idiopathic arthritis (JIA).

51 patients with juvenile idiopathic arthritis (JIA).

52 eases such as juvenile idiopathic arthritis (JIA).

53 polyarticular juvenile idiopathic arthritis (JIA).

54 e immunity in juvenile idiopathic arthritis (JIA).

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

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

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

58 We also observed associations between JIA and both STAT4 (OR 1.24 [95% CI 1.02-1.51], P = 0.02

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 After stratification by JIA subtype, the TNFAIP3 and C12orf30 variants were asso

65 nced by functional disability rather than by JIA subtype.

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

67 ch and clinical care in polyarticular-course JIA.

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

69 ignificantly robust genetic associations for JIA.

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

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

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

73 me to identify novel susceptibility loci for JIA.

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

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

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

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

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

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

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 t, plasma BLyS protein levels were normal in JIA despite blood leukocyte BLyS mRNA levels being eleva

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

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

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

99 sed on preliminary criteria for remission in JIA.

100 ciations between MTXGlu and drug response in JIA.

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

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

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

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

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

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

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

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

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

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

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

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

113 file in children with selected categories of JIA.

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

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

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

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

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

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

120 ibiotic exposure in the later development of JIA.

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

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

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

124 phages were purified from synovial fluids of JIA patients.

125 association approach to the investigation of JIA.

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

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

128 bodies may contribute to the pathogenesis of JIA.

129 bodies may contribute to the pathogenesis of JIA.

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

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

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

133 probands with JIA have an increased risk of JIA.

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

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

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

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

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

139 otein expression according to the subtype of JIA.

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

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

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

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

144 ression differs in the different subtypes of JIA.

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

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

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

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

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

150 processes may lead to improved treatment of JIA.

151 egative polyarticular JIA and oligoarticular JIA.

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

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

154 is is most common in extended oligoarticular JIA.

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

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

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

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

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

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

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

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

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

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

165 1104, found in the group with oligoarticular JIA and the group of younger patients with polyarticular

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

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

168 variants were associated with oligoarticular JIA, while the STAT4 variant was associated primarily wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 ies persisted in children with polyarticular JIA even after disease remission was achieved.

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

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

186 For children with polyarticular JIA treated for 12 months with biologic agents, 7 (25.9%

187 es; and children (n = 31) with polyarticular JIA treated with biologic agents for 12 months.

188 group of younger patients with polyarticular JIA.

189 rticular JIA and patients with polyarticular JIA.

190 nger subgroup of patients with polyarticular JIA.

191 was associated primarily 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 pressed probe sets were identified among the JIA subtypes and controls (by analysis of variance; fals

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

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

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

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

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

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

230 25 gene was significantly associated with UK JIA cases (OR for the allele 0.76 [95% CI 0.66-0.88], P

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

232 ch communities particularly in understanding JIA etiology.

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

234 l abilities in children and adolescents with JIA.

235 ease variables for employment in adults with JIA.

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

237 genotypes were analyzed for association with JIA and JIA subtypes.

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 others and fathers (n = 82) of children with JIA completed ratings of their child's symptoms, QOL, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 A substantial percentage of patients with JIA who report no or mild clinical symptoms experience s

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 r the occurrence of uveitis in patients with JIA.

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

292 to aid decision making by young people with JIA.

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

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

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

296 a database of patients ages 2-18 years with JIA (n = 524; patient visits [PV] = 2,354): visits (PV =

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.