ライフサイエンスコーパス: SLE

1 SLE patients CD4(+) T-cells that expressed CD25, CD69, a

2 SLE pregnancies are complicated due to risk for maternal

3 SLE progression (but not onset) does not require the par

4 Metabolic profiling of sera obtained from 22 SLE patients, 40 LN patients and 30 healthy controls (HC

5 lexes was measured in a cross-section of 228 SLE patients to evaluate the role of these RNA molecules

6 There were 50 249 SLE deaths and 100 851 288 non-SLE deaths from 1968 thro

7 ize MPs more completely, we investigated 280 SLE patients and 280 individually matched controls.

8 association study with replication in 4,478 SLE cases and 12,656 controls from six East Asian cohort

9 ed in purified leukocytes from 23 APS and 64 SLE patients, and 56 healthy donors.

10 ve loci, as well as joint analyses on all 82 SLE loci.

11 f the correlated (r2 > 0.8) SNPs from the 82 SLE loci were implicated in differential expression (9.8

12 toantibodies, what allows scoring accurately SLE patients.

13 thway is observed in individuals with active SLE, although the association of specific autoantibodies

14 rs of NCF1 predispose to and protect against SLE, respectively.

15 Mesenchymal stem cells (MSCs) ameliorate SLE symptoms by targeting T cells, whereas the mechanism

16 or a single antibiotic vancomycin ameliorate SLE-like disease in MRL/lpr mice by changing the composi

17 vity and specificity to distinguish LN among SLE patients and has the potential to be a useful adjunc

18 An SLE specific chromatin accessibility signature was ident

19 e disease and Def6 has been identified as an SLE risk variant.

20 ibodies to DNA and chromatin, followed by an SLE-like disease.

21 ation, and mice deficient in ETS1 develop an SLE-like autoimmunity.

22 nificantly altered in neutrophils of APS and SLE patients, is associated to their atherothrombotic st

23 ement in atherothrombosis related to APS and SLE patients.

24 croRNAs in neutrophils were lower in APS and SLE than in healthy donors.

25 racterize microRNAs linked to CVD in APS and SLE; 2) assess the effects of specific autoantibodies.

26 iency causes anti-nuclear autoantibodies and SLE disease.

27 Blood from healthy donors and SLE patients have similar circulating levels of IL-2, wh

28 ges (HMDMs) obtained from healthy donors and SLE patients.

29 s CD33/LAIR-1 expression on both healthy and SLE cells suggesting further biological control of C1q-C

30 ion, novel risk loci shared between IgAN and SLE/LN were identified, which may shed new light to expl

31 e by FXa that was potentiated by APS-IgG and SLE/APS- IgG compared to healthy control subjects' IgG,

32 APS-IgG and SLE/APS- IgG increased FXa mediated NFkappaB signalling

33 Pharmacokinetic and SLE model studies demonstrated that peptidomimetic FISLE

34 t was associated with multiple sclerosis and SLE, and its effects were clarified at the population, c

35 more efficient extraction than both SFE and SLE.

36 ssociated with multiple sclerosis as well as SLE.

37 teria from the gut microbiota and attenuated SLE-like disease in lupus-prone mice.

38 Because SLE is >/=10 times more common in women, a role for estr

39 xpected nucleotide sequence homology between SLE patient-derived autoantibodies against complement C1

40 fferentiation of monocytes into MACs in both SLE and in a model using the prototypic SLE cytokine, in

41 In 3 cases, SLE symptoms remained relatively mild after the start of

42 , rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenes

43 Allo-HSCT can cure SLE in human C1q deficiency and should be considered ear

44 ion, preserved kidney histology, and delayed SLE onset in NZB/W F1 mice.

45 associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE

46 ining PTP (SHP2), have been shown to develop SLE, suggesting a functional correlation between phospha

47 ould be a potential mechanism for developing SLE therapeutics.

48 the body are linked to a risk for developing SLE.

49 multivariate analysis, we could distinguish SLE and LN patients from HC and LN from SLE patients.

50 patients with systemic lupus erythematosus (SLE) and correlate with the occurrence of proliferative

51 ssociated with systemic lupus erythematosus (SLE) and increased susceptibility to severe bacterial in

52 Patients with systemic lupus erythematosus (SLE) and primary Sjogren's syndrome (pSS) are typically

53 orders such as systemic lupus erythematosus (SLE) and Sjogren's syndrome (SS).

54 patients with systemic lupus erythematosus (SLE) as compared with healthy controls.

55 lpha source in systemic lupus erythematosus (SLE) but their phenotype and function in different disea

56 patients with systemic lupus erythematosus (SLE) display a number of abnormalities, including increa

57 Systemic lupus erythematosus (SLE) has a strong but incompletely understood genetic ar

58 Patients with systemic lupus erythematosus (SLE) have accelerated cardiovascular disease and dysfunc

59 sk alleles for systemic lupus erythematosus (SLE) have now been identified.

60 Systemic lupus erythematosus (SLE) is a chronic, life-threatening autoimmune disorder,

61 Systemic lupus erythematosus (SLE) is a devastating multisystemic autoimmune disorder.

62 Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease with a strong

63 Systemic lupus erythematosus (SLE) is a known risk factor for endothelial dysfunction.

64 Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characterized b

65 Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with a broad sp

66 Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by

67 Systemic lupus erythematosus (SLE) is a severe autoimmune disease that is associated w

68 Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of t

69 Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and eth

70 Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by a breakd

71 Systemic lupus erythematosus (SLE) is an incurable autoimmune disease characterized by

72 Systemic lupus erythematosus (SLE) is associated with an elevated risk of vascular com

73 Systemic lupus erythematosus (SLE) is characterized by aberrant T-cell activation and

74 Systemic lupus erythematosus (SLE) is characterized by both continuous and cyclic stim

75 athogenesis of systemic lupus erythematosus (SLE) is unclear.

76 e been done on systemic lupus erythematosus (SLE) mortality trends in the United States.

77 is reduced in systemic lupus erythematosus (SLE) myelomonocytes.

78 ts compared to systemic lupus erythematosus (SLE) non APS IgG.

79 reminiscent of systemic lupus erythematosus (SLE) occurs in its absence.

80 in a cohort of systemic lupus erythematosus (SLE) patients (N = 47) and controls (N = 56).

81 ial cells from systemic lupus erythematosus (SLE) patients expressed CD95L and that after cleavage, c

82 (+) T-cells in systemic lupus erythematosus (SLE) patients show altered T-cell receptor signaling, wh

83 e B cells from Systemic Lupus Erythematosus (SLE) patients undergoing disease flares.

84 re elevated in systemic lupus erythematosus (SLE) patients, but it is not clear whether this associat

85 ssociated with systemic lupus erythematosus (SLE) susceptibility by a recent genome-wide association

86 ssociated with Systemic Lupus Erythematosus (SLE) through the integration of GWAS and eQTL data from

87 drome (ES), or systemic lupus erythematosus (SLE), and most achieved a CR (N = 8), although the time

88 eases, such as systemic lupus erythematosus (SLE), but the natural history of autoreactive GCs remain

89 unity, such as systemic lupus erythematosus (SLE), by helping B cells.

90 , most notably systemic lupus erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well as

91 that in human systemic lupus erythematosus (SLE), IgE antibodies specific for double-stranded DNA (d

92 In systemic lupus erythematosus (SLE), many self-antigens are found in apoptotic cells (A

93 ses, including systemic lupus erythematosus (SLE), Sjogren's syndrome, inflammatory bowel disease and

94 In systemic lupus erythematosus (SLE), this cross-talk was compromised; pDCs promoted pla

95 seases such as systemic lupus erythematosus (SLE), where nucleic acid-containing immune complexes (IC

96 patients with systemic lupus erythematosus (SLE), with or without glomerulonephritis; and to correla

97 hich resembled systemic lupus erythematosus (SLE)-like autoimmune disease.

98 fl)) develop a systemic lupus erythematosus (SLE)-like disease that mirrors aged Bim(-/-) mice, inclu

99 c hallmarks of systemic lupus erythematosus (SLE).

100 ion testing in systemic lupus erythematosus (SLE).

101 athogenesis of systemic lupus erythematosus (SLE).

102 of women with systemic lupus erythematosus (SLE).

103 hritis (RA) or systemic lupus erythematosus (SLE).

104 utoimmunity in systemic lupus erythematosus (SLE).

105 athogenesis of systemic lupus erythematosus (SLE).

106 immune disease systemic lupus erythematosus (SLE).

107 he hallmark of systemic lupus erythematosus (SLE).

108 marks of human systemic lupus erythematosus (SLE).

109 ceptibility to systemic lupus erythematosus (SLE).

110 a hallmark of systemic lupus erythematosus (SLE).

111 e diagnosis of Systemic Lupus Erythematosus (SLE).

112 patients with systemic lupus erythematosus (SLE).

113 with risk for systemic lupus erythematosus (SLE).

114 eases, such as systemic lupus erythematosus (SLE).

115 rine models of systemic lupus erythematosus (SLE).

116 d prognosis of Systemic Lupus Erythematosus (SLE).

117 ell-controlled systemic lupus erythematosus (SLE).

118 omplication of systemic lupus erythematosus (SLE).

119 ified IgAN and systemic lupus erythematosus (SLE)/lupus nephritis (LN) shared many loci based on GWAS

120 h the risk for systemic lupus erythematosus (SLE); however, it is unclear how Ox40L contributes to SL

121 ssociated with systemic lupus erythematosus (SLE); however, it remains unclear whether they initiate

122 Systemic lupus erythematosus (SLE; OMIM 152700) is a genetically complex autoimmune di

123 nifestations of systemic lupus erythematous (SLE).

124 Distinctive seizure-like events (SLEs) are induced in the olfactory regions by acute trea

125 and a conventional solid liquid extraction (SLE) method, showing that CXE enables faster and more ef

126 ld be an attractive therapeutic approach for SLE treatment.

127 age-standardized mortality rates (ASMRs) for SLE and non-SLE causes by sex, race/ethnicity, and geogr

128 and activated cells, i.e. pivotal events for SLE pathogenesis.

129 ponse to self-antigens with implications for SLE development therapy.

130 e majority of genetic risk polymorphisms for SLE are contained within the same regions across both po

131 and LAP, as markers of a predisposition for SLE.

132 orted loci and are possible drug targets for SLE therapeutics.

133 uish SLE and LN patients from HC and LN from SLE patients.

134 , ex vivo derived activated neutrophils from SLE patients demonstrated a similar cleavage of FcgRIIA

135 In this study, we show that PBMCs from SLE patients experiencing active disease, and hematopoie

136 he microarrays to analyze serum samples from SLE patients and found individuals with high chemokine s

137 Plasma samples from SLE positive patients were analyzed using the new FIDA m

138 % prevalence, >/=5.8-fold higher than in HDs/SLE, and significantly higher levels (p < 0.0001).

139 rsons, and residents of the South had higher SLE ASMRs and larger cumulative increases in the ratio o

140 ibody clones and serum antibodies from human SLE patients bind to DNASE1L3-sensitive chromatin on the

141 presents a novel therapeutic target in human SLE.

142 In SLE patients treated with cholecalciferol for 12 weeks,

143 In SLE T cells, SAP protein is also subject to increased de

144 f phenotype, are 2-10 times more abundant in SLE blood compared to controls.

145 When added in SLE T cell in vitro cultures, IL-23 induced IL-17 and li

146 ese data suggest that type I IFN blockade in SLE and pSS patients will lead to downregulation of BAFF

147 factors in memory, DN, and naive B cells in SLE show elevated levels of Aiolos, whereas Ikaros level

148 al dysfunction and cardiovascular disease in SLE.

149 netic architecture and ethnic disparities in SLE.

150 ) MPs, suggests a generalized disturbance in SLE.

151 FN-alpha promotes endothelial dysfunction in SLE, focusing on its regulation of eNOS and NO productio

152 ls, are associated with IFN dysregulation in SLE.

153 of the genetic control of gene-expression in SLE by maximising the leverage of RNA-Seq and performing

154 on occurs and contributes to renal injury in SLE.

155 -gamma and IL-17A/F, 2 cytokines involved in SLE-associated organ damage.

156 Restoration of SAP levels in SLE T cells corrects the overexcitable lupus T cell phen

157 y identified 10 new and 6 suggestive loci in SLE.

158 ic and the regulatory role of lymphocytes in SLE beyond the production of IgG autoantibodies.

159 ment of kidney damage and rapid mortality in SLE mice.

160 nd STAT1-STAT3 activation were normalized in SLE patients responding to rituximab.

161 sion of CD24(+)CD38(hi) Breg cell numbers in SLE was associated with altered STAT1 and STAT3 activati

162 PS(-) MPs predominated in SLE, but not in controls (66% vs. 42%).

163 this study, we show that the ICs present in SLE patients by ligating to FcgammaRIIIa on CD4(+) T-cel

164 terogeneity among autoantibodies produced in SLE.

165 nce for an altered epigenetic programming in SLE B cells and identify loci and transcription factor n

166 significantly (P < 0.05) over-represented in SLE loci, consistent with apoptosis playing a critical r

167 leptin in modulating autoimmune responses in SLE can open possibilities of leptin-targeted therapeuti

168 nt with apoptosis playing a critical role in SLE.

169 Forced expression of SAP in SLE T cells normalized IL-2 production, calcium (Ca(2+))

170 drivers of the inflammatory changes seen in SLE.

171 Selectively in SLE, PS(-) MPs were more numerous in females and smokers

172 sociated with increased clinical severity in SLE patients, and a study of the cellular source of IFNa

173 of proinflammatory cytokines was similar in SLE patient-derived cells, with the exception that IL-10

174 Previous MP studies in SLE have been limited in size and differ regarding numbe

175 AMF3 acts as potential therapeutic target in SLE patients by augmenting sensitivity to IL-2.

176 er, in the chronic model of pristane-induced SLE, IL-17F-deficient mice developed less severe disease

177 from six East Asian cohorts to identify new SLE susceptibility loci and better localize known loci.

178 e were 50 249 SLE deaths and 100 851 288 non-SLE deaths from 1968 through 2013.

179 ized mortality rates (ASMRs) for SLE and non-SLE causes by sex, race/ethnicity, and geographic region

180 increases in the ratio of the SLE to the non-SLE ASMR (31.4%, 62.5%, and 58.6%, respectively) than ma

181 The non-SLE ASMR decreased every year starting in 1968, whereas

182 od, the SLE ASMR decreased less than the non-SLE ASMR, with a 34.6% cumulative increase in the ratio

183 d since 1968 but remain high relative to non-SLE mortality, and significant sex, racial, and regional

184 Novel SLE associated splicing events were identified in the T-

185 endent associations); these include 24 novel SLE regions (P<5 x 10(-8)), refined association signals

186 n summary, we provide evidence of five novel SLE susceptibility loci.

187 ing exon-level RNA-Seq, and identified novel SLE susceptibility genes (e.g. NADSYN1 and TCF7) that we

188 We recently identified ten novel SLE susceptibility loci in Asians and uncovered several

189 Drusen-like deposits were detected in 40% of SLE subjects and 3.33% of controls (P < .0001).

190 in 68% (68 of 100) of HDs, 69% (68 of 99) of SLE patients, and 81% (79 of 97) of RA patients.

191 racial/ethnic differences in associations of SLE mortality with sex and region.

192 The role of leptin in the development of SLE was confirmed in the New Zealand Black (NZB) x New Z

193 ficient, mice accelerated the development of SLE-like disease, including increased serum levels of au

194 pristane, also results in the development of SLE-like disease.

195 ped an in vitro model to study the effect of SLE patient-derived anti-C1q bound to immobilized C1q (i

196 The patient had no evidence of SLE and had normal complement levels.

197 Exposure of SLE neutrophils, or healthy IFN-primed neutrophils, to a

198 al retention of Ox nucleoids is a feature of SLE blood neutrophils, and autoantibodies against Ox mtD

199 es within the known biochemical framework of SLE.

200 VWF deposition in C1q-positive glomeruli of SLE patients compared with control nephropathy.

201 role of circulating RNA in a large group of SLE patients and provides an important link with IFN dys

202 nity, and autoantibodies are the hallmark of SLE.

203 loci, increase the explained heritability of SLE to 24%.

204 tudy uncovers the molecular heterogeneity of SLE and provides an explanation for the failure of clini

205 for a genetic basis of the high incidence of SLE in Asian ancestry.

206 ng Psgl-1 may be useful in the management of SLE patients at high risk of acute vascular complication

207 ted with relevant clinical manifestations of SLE, with potential for use as biomarkers in clinical pr

208 tures, suggestive of conserved mechanisms of SLE etiopathogenesis.

209 s in the NZB x NZW (NZB/W) F1 mouse model of SLE.

210 ates other TLR7-driven spontaneous models of SLE and is negatively regulated by TLR9.

211 be an important step in the pathogenesis of SLE, generating anti-nuclear antibodies and producing ty

212 teraction contributes to the pathogenesis of SLE.

213 a, and may contribute to the pathogenesis of SLE.

214 ic load) exhibits an accelerating pattern of SLE risk, leading us to posit a cumulative hit hypothesi

215 The prevalence of SLE as a cause of uveitis was estimated to be 0.47% (95%

216 s suggested that the increased prevalence of SLE in non-Europeans (including Asians) has a genetic ba

217 ke receptor (TLR) signaling in processing of SLE ICs and downstream inflammatory neutrophil effector

218 Rates of SLE mortality have decreased since 1968 but remain high

219 ata identify SHP2 as a critical regulator of SLE pathogenesis and suggest targeting of its activity a

220 ment pathway followed by reduced severity of SLE symptoms.

221 ransplantation, and clinically, all signs of SLE have resolved.

222 merged as a successful treatment strategy of SLE.

223 a large transancestral association study of SLE using Immunochip genotype data from 27,574 individua

224 further enhanced by calcitriol treatment of SLE MACs.

225 Ikaros may have utility in the treatment of SLE, where elevated levels of BAFF and Aiolos may prime

226 novel therapeutic target in the treatment of SLE.

227 cates may have resulted in underestimates of SLE ASMRs.

228 Limitations: Underreporting of SLE on death certificates may have resulted in underesti

229 Ligation of SLAMF3 receptors on SLE CD4(+) T cells restores IL-2 responses to levels com

230 a reactive IgG from patients with APS and/or SLE potentiate this effect.

231 r FXa reactive IgG from patients with APS or SLE/APS- alter these responses.

232 s better discriminated between RA and HDs or SLE, with significantly higher AHA levels against IgG1/3

233 arance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-1

234 Similar analyses of fifteen other SLE risk loci identified 1206 functional variants tightl

235 patients from non-nephritis lupus patients (SLE) and further to get new insights into the underlying

236 both SLE and in a model using the prototypic SLE cytokine, interferon-alpha.

237 udies showed that over half of the published SLE genetic associations are present in both populations

238 d boy and a 12-year-old girl with refractory SLE restored C1q production after allo-HSCT.

239 rm bioinformatic analyses on all 82 reported SLE loci to identify shared regulatory signatures.

240 share genetic signatures with other reported SLE loci, including effects on gene expression, transcri

241 but 2 patients developed treatment-resistant SLE, and we decided to pursue treatment with allo-HSCT.

242 Targeted sequencing of sixteen SLE risk loci among 1349 Caucasian cases and controls pr

243 n T-helper cells is critical for spontaneous SLE-like autoimmune disease development; we also reveale

244 ses of numerous murine models of spontaneous SLE have revealed a critical role for endosomal TLRs in

245 e (NZW)F1 (NZB/W) mouse model of spontaneous SLE, where elevated leptin levels correlated with diseas

246 DNASE1L3 are linked to familial and sporadic SLE, respectively.

247 derlying causal variant that drives a strong SLE-associated signal detected by the Immunochip in the

248 Although 15 times less common than SLE, NL provides a unique opportunity to study two diffe

249 We conclude that SLE T cells display reduced levels of the adaptor protei

250 We observed that SLE MACs are dysfunctional and secrete pro-inflammatory

251 We previously reported that SLE neutrophils exposed to TLR7 agonist autoantibodies r

252 The study revealed that SLE patients had significantly elevated levels of circul

253 oinformatics using all 82 loci revealed that SLE susceptibility loci share many gene regulatory featu

254 cellular potassium changes demonstrates that SLEs in the piriform cortex initiate in the superficial

255 , statistically significant increases in the SLE ASMR did not occur among white persons over the 46-y

256 Here we show that lack of the SLE risk variant Def6 results in deregulation of Bcl6 pr

257 ger cumulative increases in the ratio of the SLE to the non-SLE ASMR (31.4%, 62.5%, and 58.6%, respec

258 Over this period, the SLE ASMR decreased less than the non-SLE ASMR, with a 34

259 form of vitamin D (calcitriol) restored the SLE MAC phenotype towards that of healthy subjects with

260 sed every year starting in 1968, whereas the SLE ASMR decreased between 1968 and 1975, increased betw

261 Exposure of normal T cells to SLE serum IgG, known to contain anti-CD3/TCR Abs, result

262 Compared to SLE patients, the LN patients had increased serum levels

263 f this tolerance mechanism can contribute to SLE, and its restoration may represent a therapeutic opp

264 ever, it is unclear how Ox40L contributes to SLE pathogenesis.

265 nt and ancestry-independent contributions to SLE risk.

266 tin on the propathogenic events that lead to SLE.

267 gen species (ROS) production, predisposes to SLE (odds ratio (OR) = 3.47 in Asians (Pmeta = 3.1 x 10(

268 we compared the extent of susceptibility to SLE and lupus manifestations between leptin-deficient (o

269 ls) subjects found ten previously unreported SLE loci.

270 dation upon C1 treatment was estimated using SLE patient autoantibodies.

271 Forty-two DEGs were found when SLE cases were compared to controls, consistent with act

272 similar circulating levels of IL-2, whereas SLE patients exhibit elevated BAFF and DN B cells and re

273 leotide polymorphisms (SNPs) associated with SLE and other autoimmune diseases affect the IFN-alpha p

274 nterferon signaling pathways associated with SLE disease.

275 d population characteristics associated with SLE mortality.

276 ucing vascular complications associated with SLE.

277 ynonymous Mac-1 polymorphism associated with SLE.

278 -DR and DQ molecules on dendritic cells with SLE risk genotypes, which increases to over 4-fold after

279 olimus should be considered in children with SLE, ES, and CVID.

280 The amount of U1 and Y1 RNA complexed with SLE patient Abs and immune complexes was measured in a c

281 ood-borne RNA molecules were correlated with SLE disease activity and increased expression of IFN-ind

282 ts isolated from 32 women and three men with SLE, independent of disease activity.

283 Sixty patients with SLE (age, 18-55 years; 30 with and 30 without SLE-relate

284 oidal thickness was greater in patients with SLE (P = .002).

285 at was shown to be elevated in patients with SLE and in lupus models, was also increased in an ICOS-d

286 Notably, up to 75% of patients with SLE experience neuropsychiatric symptoms that range from

287 ippocampal brain sections from patients with SLE may instruct the evaluation of ongoing clinical tria

288 e disease, and phagocytes from patients with SLE often display defective clearance and increased infl

289 The prevalence of DLDs in patients with SLE was similar regardless of renal involvement, but pat

290 Drusen-like deposits in patients with SLE were independent of renal disease and were best dete

291 from whole kidney biopsies of patients with SLE.

292 CT should be considered in all patients with SLE.

293 ical symptoms observed in some patients with SLE.

294 ld have a therapeutic value in patients with SLE.

295 and suggest shared methylation patterns with SLE.

296 ons of demographic variables and period with SLE mortality.

297 isolated nucleoli were broadly reactive with SLE patient autoantibodies.

298 t associations of sex, race, and region with SLE mortality risk and revealed significant racial/ethni

299 nning, monitoring, and care, most women with SLE can anticipate a successful pregnancy.

300 LE (age, 18-55 years; 30 with and 30 without SLE-related glomerulonephritis) and 60 age- and sex-matc