ライフサイエンスコーパス: RRMS

1 RRMS demonstrated more pronounced deep GM atrophy in com

2 RRMS may start years prior to clinical presentation, and

3 RRMS relaxing-remitting MS patients had lower WM white m

4 RRMS was characterized by autoantibodies to heat shock p

5 RRMS was correctly diagnosed among White female vignette

6 tting MS (RRMS; mean age: CIS: 31.4 +/- 9.0; RRMS: 33.0 +/- 8.7 years; mean disease duration: CIS: 7.

7 r the curve [AUC] = 0.66 vs 0.53; p = 0.03), RRMS (AUC = 0.73 vs 0.59; p < 0.001), PMS (AUC = 0.77 vs

8 1002 RRMS patients were followed for an average of 2.6 years.

9 1106 RRMS patients were randomised 1:1 to receive once-daily

10 From among 135 RRMS patients who initiated FTY in a 2-year multicentre

11 178 RRMS, 186 PMS, and 66 control participants were followed

12 e global RNA profile of serum exosomes in 19 RRMS patients (9 in relapse, 10 in remission) and 10 HC.

13 We conducted a retrospective study in 192 RRMS patients treated with IFNbeta-1b.

14 Furthermore, low-BMI (BMI </= 23 kg/m(2)) RRMS patients show increased levels of small HDL (sHDL),

15 Thirty-five patients (20 RRMS, 15 SPMS) completed AHSCT, with a median follow-up

16 Blood from 31 RRMS and 28 SPMS patients was subjected to different sam

17 atus Scale (median, min-max): CIS: 1, 0-3.5; RRMS: 1.25, 0-4) with 3.0T magnetic resonance imaging.

18 dated using qPCR on an independent set of 50 RRMS patients, 51 SPMS patients, and 32 HCs.

19 Thirteen trials including >13,500 RRMS patients were included in the meta-analysis.

20 in reaction with an independent cohort of 63 RRMS patients (33 in relapse, 30 in remission) and 32 HC

21 es (CIS: -0.95 +/- 2.11% vs -1.19 +/- 3.67%; RRMS: -1.74 +/- 2.57% vs -1.74 +/- 4.02%; PMS: -2.29 +/-

22 EFS at 3 years was 60%, (70% RRMS).

23 d immunosorbent assay in 105 MS patients (73 RRMS, 12 primary progressive MS, 20 secondary progressiv

24 as lower for GBSI than CSA (CIS: 106 vs 830; RRMS: 95 vs 335; PMS: 44 vs 215; power = 80%; alpha = 5%

25 the majority of patients with highly active RRMS over an average seven-year follow-up.

26 efficacy and safety of alemtuzumab in active RRMS.

27 e for inducing sustained remission of active RRMS and was associated with improvements in neurologic

28 In addition, RRMS, SPMS, and PPMS were characterized by unique patter

29 on a subset of these subjects and additional RRMS (n = 4), clinically isolated syndrome (n = 2), and

30 We compared outcomes for all RRMS patients switching from natalizumab due to JC virus

31 ressive MS compared with HCs (p = 0.004) and RRMS (p = < 0.001) and correlated negatively with disabi

32 0.03; ONL:-0.12 +/- 0.06%/yr, p = 0.04), and RRMS (INL:-0.10 +/- 0.04%/yr, p = 0.01; ONL:-0.13 +/- 0.

33 D in the occipital cortex (32.83 cm(3)); and RRMS diffusely in the GM (260.61 cm(3)).

34 tion of CD8(low)CD4(-) cells in both CIS and RRMS in the absence of treatment as well as suggestive e

35 Similarities between untreated CIS and RRMS subjects extend to broader immunological profiles:

36 y of miRNAs differentiated SPMS from HCs and RRMS from SPMS.

37 hsa-miR-145 differentiated RRMS from HCs and RRMS from SPMS.

38 In MOGAD and RRMS, lesion-related tract degeneration is associated wi

39 s Scale worsening in patients with NMOSD and RRMS.

40 ed in RRMS relapse compared to remission and RRMS compared to NINDC, respectively.

41 differences in MRI measures between SPMS and RRMS were the number of cortical lesions, which were hig

42 It was different in RRMS versus SPMS, and RRMS versus HCs, and showed an association with EDSS and

43 ons (SPMS 1.4 (1.8) per person per year, and RRMS 1.1 (1.0)), and none arose de novo, or from previou

44 was found in the NMOSD (5.4+/-8.2 years) and RRMS (13.0+/-14.7 years) groups compared with healthy co

45 sed protocol remained discriminatory between RRMS and SPMS despite these sample-handling variations.

46 nhancing lesions on brain MRI scans for both RRMS studies.

47 ase-inducing leukocytes into the CNS in both RRMS and PMS and suggest that blocking DICAM with a mono

48 ive lesions were found in patients with both RRMS and SPMS.

49 re similar for relapsing-remitting MS cases (RRMS), those developing primary-progressive MS (PPMS) sc

50 patients to one of two diagnosis categories, RRMS or other neurological disease, with 87% accuracy by

51 ave multifocal disease at onset, and develop RRMS by follow-up.

52 -based statistical classifier for diagnosing RRMS that provides a high degree of diagnostic capabilit

53 MS from SPMS, and hsa-miR-145 differentiated RRMS from HCs and RRMS from SPMS.

54 hsa-miR-454 differentiated RRMS from SPMS, and hsa-miR-145 differentiated RRMS from

55 t the brain MRI criteria for differentiating RRMS from NMOSD are sensitive and specific for all pheno

56 mab improves ambulatory function in disabled RRMS subjects and may have efficacy in disabled SPMS sub

57 This test remained able to discriminate RRMS and SPMS samples that had experienced additional fr

58 hat begins as a relapsing-remitting disease (RRMS) and is followed by a progressive phase (SPMS).

59 ed that serum metabolomics could distinguish RRMS from SPMS with high diagnostic accuracy.

60 stribution criteria were able to distinguish RRMS with a sensitivity of 90.9% and with a specificity

61 que autoantibody patterns that distinguished RRMS, secondary progressive (SPMS), and primary progress

62 treatment-naive patients with active, early RRMS were randomly assigned in a 1:1:1 ratio to receive

63 ve MS plaques predominate in acute and early RRMS and are the likely substrate of clinical attacks.

64 uding clinically isolated syndrome and early RRMS.

65 rs in the pivotal trial of IM IFNbeta-1a for RRMS was conducted.

66 chanisms of action of the approved drugs for RRMS provide a strong foundation for understanding the p

67 g Administration approval as a treatment for RRMS.

68 ted amyotrophic lateral sclerosis (ALS) from RRMS subjects, but were not different between SPMS and A

69 We found that memory and naive B cells from RRMS and secondary progressive MS patients exhibited a s

70 T and CD4(+)RORgammat(+) T (Th17) cells from RRMS subjects that associated with an increased migrator

71 he study was performed on blood samples from RRMS patients enrolled in the CARE-MS II clinical trial,

72 ad relapsing-remitting MS (RRMS), 3 (4%) had RRMS and EDSS scores >3.5, 26 (34%) had secondary progre

73 PN1 comprised 10 hubs in HCs, RRMS and PPMS but did not include the right thalamus in

74 In RRMS patients, IFN-beta nonresponders had higher IL-17F

75 In RRMS, lesion accumulation rate was associated with GCIP

76 In RRMS, the diffuse GM atrophy was associated with lesions

77 In RRMS, the presence of CSF OCBs predicts shorter time to

78 In RRMS, the presence of CSF oligoclonal bands (OCBs) was a

79 In RRMS, the treatment effect on brain atrophy is correlate

80 ased time to moderate disability (EDSS 4) in RRMS (HR=0.774 (95% CI, 0.632 to 0.948), p=0.013).

81 ive MS, increased during disease activity in RRMS but is unaffected by treatment of highly active DMT

82 short-term inflammatory disease activity in RRMS.

83 poprotein levels and function are altered in RRMS patients, especially in low-BMI patients, which may

84 s detected, 60 were significantly altered in RRMS.

85 expressed in RRMS and SPMS versus HCs and in RRMS versus SPMS.

86 rain (and additionally GM and WM) atrophy in RRMS increased incrementally with step-wise refinement t

87 ted for 62% of the variance in GM atrophy in RRMS, but there were no significant predictors of GM atr

88 uration was associated with increased BAG in RRMS.

89 gnificantly correlated with decreased CMT in RRMS (r = -0.295; p = 0.015), but not in CIS (r = 0.032;

90 lly expressed PBMC sncRNAs were decreased in RRMS compared to NINDC.

91 ol of structural RNAs, are also deficient in RRMS.

92 r atrophy indicate that mechanisms differ in RRMS and SPMS.

93 It was different in RRMS versus SPMS, and RRMS versus HCs, and showed an ass

94 reliable markers of permanent disability in RRMS trials.

95 s differential methylation is not evident in RRMS, making it a potential biomarker of progressive dis

96 ects in structural RNA surveillance exist in RRMS and establish a causal link between Ro60 and La pro

97 ating miRNAs are differentially expressed in RRMS and SPMS versus HCs and in RRMS versus SPMS.

98 NA category were differentially expressed in RRMS patients versus HC: hsa-miR-122-5p, hsa-miR-196b-5p

99 iR-92) that were differentially expressed in RRMS versus SPMS also differentiated amyotrophic lateral

100 croRNAs (miRNAs) differentially expressed in RRMS.

101 ntial to improve fatigue and fatigability in RRMS.

102 nts) comparing directly INFbeta versus GA in RRMS.

103 ivity is becoming a viable treatment goal in RRMS; we therefore aimed to assess the effects of cladri

104 ammonis (CA) 1 region of the hippocampus in RRMS with further worsening of CA1 loss and extension in

105 ear cells was also significantly impaired in RRMS.

106 ssemination in time on MRI) and increased in RRMS patients in two clinically relevant networks subser

107 entially expressed sncRNAs were increased in RRMS relapse compared to remission and RRMS compared to

108 Interestingly, in RRMS CSF GAP-43 levels were higher in patients with sign

109 We observed smaller LDL in RRMS patients compared to healthy controls and to progre

110 Improving clinical outcomes in RRMS requires both a better understanding of the immunol

111 tify impaired disease resolution pathways in RRMS caused by dysregulated ANXA1 expression that could

112 cs to CD8(+) cells isolated from patients in RRMS, identifying a signature reflecting expansion of a

113 reduced CD40-mediated P65 phosphorylation in RRMS patients, suggesting that reducing CD40-mediated p-

114 e more destructive pathological processes in RRMS patients.

115 ting exosomes have a distinct RNA profile in RRMS.

116 red capacity of Treg cells to proliferate in RRMS correlates with the clinical state of the subject,

117 as significantly decreased during relapse in RRMS.

118 important measure of therapeutic response in RRMS.

119 efects in surveillance of structural RNAs in RRMS exemplified by elevated levels of poly(A) + Y1-RNA,

120 The independent predictors of EDSS score in RRMS were lateral funiculi FA, normalized brain volume,

121 /yr, p = 0.01), whereas they were similar in RRMS and controls.

122 present new potential therapeutic targets in RRMS.

123 t not the other markers, were higher than in RRMS and correlated with actual clinical disability scor

124 significantly more abnormal in SPMS than in RRMS.

125 across the brain was greater in SPMS than in RRMS.

126 ed trials (RCTs) of natalizumab treatment in RRMS to investigate the association of age and inflammat

127 en deciding on immunomodulatory treatment in RRMS.

128 all published randomized clinical trials in RRMS lasting at least 2 years and including as endpoints

129 GM atrophy is more widespread in RRMS compared with the other two conditions.

130 ation about subsequent clinical worsening in RRMS.

131 y have prognostic value, over many years, in RRMS.

132 ability Status Scale score >/=3.5, including RRMS subjects from the phase 3 AFFIRM and SENTINEL trial

133 ase compared with relapsing-remitting males (RRMS) and female MS subjects, with increased levels of C

134 f PPMS based on high fulfillment of modified RRMS DIS criteria had high specificity, but low sensitiv

135 an disease duration: CIS: 7.2 +/- 15 months; RRMS: 8.0 +/- 6.5 years, Expanded Disability Status Scal

136 fecal microbiota in relapsing remitting MS (RRMS) (n = 31) patients to that of age- and gender-match

137 ppocampal volumes in relapsing remitting MS (RRMS) and secondary progressive MS (SPMS) patients and c

138 r of regeneration in relapsing-remitting MS (RRMS) and whether disease-modifying therapies (DMTs) inf

139 Patients with relapsing-remitting MS (RRMS) or clinically isolated syndrome (CIS) with disease

140 ic acid plasma in 10 relapsing-remitting MS (RRMS) patients, 9 secondary progressive MS (SPMS) patien

141 (SPMS) patients, 12 relapsing-remitting MS (RRMS) patients, and 14 matched healthy controls underwen

142 em, progressing from Relapsing-Remitting MS (RRMS) to Secondary Progressive MS (SPMS) in many cases.

143 ed syndrome (CIS) or relapsing-remitting MS (RRMS) to SPMS.

144 acute monophasic and relapsing-remitting MS (RRMS) were active.

145 diffusion data in 58 relapsing-remitting MS (RRMS), 28 primary progressive MS (PPMS), 36 secondary pr

146 .5), all of whom had relapsing-remitting MS (RRMS), 3 (4%) had RRMS and EDSS scores >3.5, 26 (34%) ha

147 effector function in relapsing/remitting MS (RRMS), an autoimmune disease sustained by proinflammator

148 es, 36 patients with relapsing-remitting MS (RRMS), and 27 patients with secondary progressive MS (SP

149 38) in patients with relapsing-remitting MS (RRMS), compared with patients with chronic progressive M

150 ion is a hallmark of relapsing-remitting MS (RRMS), PMS is associated with chronic, tissue-restricted

151 t MS subtypes, i.e., relapsing-remitting MS (RRMS), secondary-progressive MS (SPMS), and primary-prog

152 y remissions, called relapsing-remitting MS (RRMS).

153 reated subjects with relapsing-remitting MS (RRMS).

154 3) were persons with relapsing-remitting MS (RRMS).

155 me (CIS) and 69 with relapsing-remitting MS (RRMS; mean age: CIS: 31.4 +/- 9.0; RRMS: 33.0 +/- 8.7 ye

156 d from subjects with relapsing-remitting MS (RRMS; n = 12), other neurologic diseases (ONDs; n = 1),

157 .67; p < 0.001) than relapsing-remitting MS (RRMS; r = 0.33; p = 0.007).

158 97 patients (61 with relapsing-remitting MS [RRMS] and 36 with progressive MS) and 44 healthy control

159 nts with MS (58 with relapsing-remitting MS [RRMS] and 62 with progressive MS [PMS]) and 30 age- and

160 e MS [SPMS], 27 with relapsing remitting MS [RRMS]) and 30 healthy volunteers, genetically stratified

161 (AC), 47 HAM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary progressive MS [SPMS], and 40 primar

162 syndrome [CIS], 196 relapsing-remitting MS [RRMS], 34 progressive MS [PMS]), and 82 controls from 8

163 forty-seven pwMS (330 relapsing-remitting MS-RRMS and 117 progressive MS-PMS) were recruited.

164 348 plasma and 131 sera from treatment-naive RRMS patients (n=52), healthy controls (n=23) and a plac

165 data included patients with MOGAD/AQP4+NMOSD/RRMS in non-acute disease stage.

166 n with 70% of SPMS sera compared with 25% of RRMS sera (P < 0.001).

167 ostic biochemical motif in the antibodies of RRMS patients, which may offer insight into the disease

168 he hyperphosphorylation of P65 in B cells of RRMS patients at levels similar to healthy donor control

169 f PPMS is more challenging than diagnosis of RRMS.

170 e activity (clinical and/or radiological) of RRMS.

171 d that the endogenous IFN-beta from serum of RRMS patients induced a significantly lower IFN-inducibl

172 estigation of ponesimod for the treatment of RRMS is under consideration.

173 e and effective regimen for the treatment of RRMS, providing the convenience of fewer sc injections p

174 ere are nine approved drugs for treatment of RRMS.

175 e was associated with conversion from CIS or RRMS to SPMS (+26.4 mm(3); 95% CI: 4.2 mm(3), 56.9 mm(3)

176 treatment of clinically isolated syndrome or RRMS males with a high-expresser genotype might slow or

177 219 patients with paediatric RRMS or CIS were enrolled.

178 mmatory (51 relapsing remitting MS patients (RRMS)), and neuro-degenerative (34 Alzheimer's disease p

179 ubsets and its contribution to the prolonged RRMS suppression following alemtuzumab-induced lymphocyt

180 or patients with active relapsing remitting (RRMS) and secondary progressive MS (SPMS).

181 t in a third cohorts of relapsing-remitting (RRMS) patients.

182 n independent cohort of relapsing-remitting (RRMS) samples.

183 progressive (SPMS) and relapsing-remitting (RRMS) subgroups.

184 and cell-free CSF from relapsing-remitting (RRMS, n = 12 in relapse and n = 11 in remission) patient

185 cases characterised by relapsing/remitting (RRMS) attacks of neurologic dysfunction followed by vari

186 relapsing-remitting MS multiple sclerosis ( RRMS relaxing-remitting MS ) patients, and 12 secondary

187 t of relapsing-remitting multiple sclerosis (RRMS) and AQP4-ab NMOSD patients and also assessed their

188 s in relapsing remitting multiple sclerosis (RRMS) and other inflammatory diseases.

189 with relapsing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS

190 e in relapsing-remitting multiple sclerosis (RRMS) are lacking.

191 for relapsing-remitting multiple sclerosis (RRMS) are only partly effective -- breakthrough disease

192 with relapsing remitting multiple sclerosis (RRMS) as compared to healthy control individuals.

193 with relapsing-remitting multiple sclerosis (RRMS) because of altered interleukin-2 (IL-2) secretion

194 with relapsing-remitting multiple sclerosis (RRMS) by high-dimensional single-cell mass cytometry (Cy

195 y in relapsing-remitting multiple sclerosis (RRMS) diminishes with increasing age.

196 with relapsing-remitting multiple sclerosis (RRMS) have an increased frequency of IL-11(+) monocytes,

197 with relapsing remitting multiple sclerosis (RRMS) have higher replacement mutation frequencies than

198 tive relapsing-remitting multiple sclerosis (RRMS) in Europe, which in phase II and III studies demon

199 y in relapsing-remitting multiple sclerosis (RRMS) is not well understood, but induction of apoptosis

200 e in relapsing-remitting multiple sclerosis (RRMS) is prognostically crucial, yet robust comparative

201 with relapsing-remitting multiple sclerosis (RRMS) markedly prevents new MRI-detected lesions and dis

202 with relapsing-remitting multiple sclerosis (RRMS) or secondary progressive multiple sclerosis (SPMS)

203 for relapsing-remitting multiple sclerosis (RRMS) over an extended follow-up are lacking.

204 e in relapsing-remitting multiple sclerosis (RRMS) patients and healthy controls (HC).

205 from relapsing-remitting multiple sclerosis (RRMS) patients exhibited enhanced proliferation with CD4

206 tive relapsing-remitting multiple sclerosis (RRMS) patients who are stable on natalizumab switch to o

207 from relapsing-remitting multiple sclerosis (RRMS) patients.

208 the relapsing-remitting multiple sclerosis (RRMS) population, 30-50% of MS patients are non-responsi

209 with relapsing-remitting multiple sclerosis (RRMS) showed that short-course oral treatment with cladr

210 with relapsing-remitting multiple sclerosis (RRMS) to assess the drug's safety, efficacy, and pharmac

211 from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive MS (SPMS) represents a hu

212 ent of relapse remitting multiple sclerosis (RRMS), 2 offers several potential advantages having demo

213 with relapsing-remitting multiple sclerosis (RRMS), alemtuzumab reduced relapse rate and the risk of

214 for relapsing-remitting multiple sclerosis (RRMS), but no published randomised trials have directly

215 y in relapsing-remitting multiple sclerosis (RRMS), oral laquinimod slowed disability and brain atrop

216 with relapsing-remitting multiple sclerosis (RRMS), TRANSFORMS, fingolimod showed greater efficacy on

217 with relapsing-remitting multiple sclerosis (RRMS).

218 s in relapsing-remitting multiple sclerosis (RRMS).

219 with relapsing-remitting multiple sclerosis (RRMS).

220 for relapsing-remitting multiple sclerosis (RRMS).

221 n in relapsing-remitting multiple sclerosis (RRMS).

222 for relapsing-remitting multiple sclerosis (RRMS).

223 and relapsing-remitting multiple sclerosis (RRMS).

224 with relapsing-remitting multiple sclerosis (RRMS).

225 n in relapsing-remitting multiple sclerosis (RRMS).

226 relapsing and remitting multiple sclerosis (RRMS).

227 from relapsing-remitting multiple sclerosis (RRMS).

228 t of relapsing-remitting multiple sclerosis (RRMS); however, several clinical trials have shown that

229 Compared to HC, CIS and (even more so) RRMS patients demonstrated significantly reduced CMT.

230 rituximab compared with fingolimod in stable RRMS patients who switch from natalizumab due to JC viru

231 urther, paired CSF and blood B cell subsets (RRMS; n = 7) were isolated using fluorescence activated

232 re inactive in patients with SPMS (35%) than RRMS (23%), but active lesions were found in all patient

233 er year was greater in SPMS (1.6 (1.9)) than RRMS (0.8 (1.9)) (Mann-Whitney p=0.039).

234 played greater occipital cortex atrophy than RRMS (19.82 cm(3)).

235 more pronounced temporal cortex atrophy than RRMS (6.71 cm(3)), whereas AQP4+NMOSD displayed greater

236 ervative threshold, lower diffusivities than RRMS patients in distinct cerebral associative, commissu

237 ation appears to be more common in SPMS than RRMS.

238 For the RRMS studies, an open-label phase I study found that rit

239 blood tests, the results confirmed that the RRMS vs. SPMS test is resistant to sample-handling varia

240 .07%/yr, p < 0.001) thinning, as compared to RRMS.

241 ly isolated syndromes patients converting to RRMS to 14-fold normal in SPMS.

242 We applied our method to RRMS, an autoimmune disease that is notoriously difficul

243 ndary progressive MS was reduced relative to RRMS relaxing-remitting MS in WM white matter , GM gray

244 s neuromyelitis optica, a disease similar to RRMS.

245 In this cohort of actively treated RRMS, patients' processing speed remained stable over th

246 this cohort of people with actively treated RRMS, self-reported fatigue remained stable or increased

247 ession levels of ANXA1 in naive-to-treatment RRMS subjects inversely correlated with disease score an

248 of all disability accrual events in typical RRMS.

249 Unlike RRMS, disease-modifying therapies (DMTs) did not impact

250 ry disease activity in treated and untreated RRMS.

251 d as being reduced in frequency in untreated RRMS subjects (P = 0.0002), and this observation was con

252 lood whose frequency is altered in untreated RRMS subjects.

253 are three distinct populations of untreated RRMS subjects and that these distinct phenotypic categor

254 d WexInc were significantly higher in PMS vs RRMS (p < 0.001), and significantly associated with dise

255 A total of 1400 patients, 971 with RRMS (median age, 39.14 years [IQR, 31.38-46.80 years];

256 lity study in people recently diagnosed with RRMS and fatigue, throughout the Thames Valley, UK (ISRC

257 23 236 eligible patients were diagnosed with RRMS or clinically isolated syndrome.

258 A total of 418 patients with RRMS (43.0%) and 226 with PMS (52.7%) were treated with

259 rols and marginally reduced in patients with RRMS (mean [SD] level, 682 [173] nM; P = .04), whereas p

260 85 patients with NMOSD and 124 patients with RRMS (mean duration NMOSD=5.8+/-1.9 (1.9-9.9) years, RRM

261 [101] nM; P = 9.55 x 10-9) and patients with RRMS (P = 1.83 x 10-4).

262 ith annualized relapse rate in patients with RRMS (r = 0.37; 95% CI: 0.1, 0.55; P = .005).

263 CP volume in patients with RRMS (r = 0.57; 95% CI: 0.37, 0.73; P = .009) correlated

264 Of 531 patients with RRMS aged 18 to 60 years screened, 266 were excluded bef

265 loring treatment to individual patients with RRMS and altering treatment in patients with breakthroug

266 s were conducted separately in patients with RRMS and PMS using propensity score-weighted logistic re

267 ness to IFN-beta therapy among patients with RRMS and, furthermore, that such differential patterns o

268 rs (S1PRMs) in treatment-naive patients with RRMS are limited.

269 proposed strategies to monitor patients with RRMS being treated with DMDs, outline approaches to iden

270 allel-group, open-label study, patients with RRMS diagnosed with the McDonald criteria who had had at

271 Thirty-six patients with RRMS from referral centers were screened; 25 were enroll

272 We found that patients with RRMS have increased serum and cerebrospinal fluid Th17 (

273 levels in natalizumab-treated patients with RRMS in clinical practice.

274 safety, and immunogenicity for patients with RRMS in the tested setting.

275 to occur in roughly 5% of all patients with RRMS per annum, causing at least 50% of all disability a

276 A total of 21 patients with RRMS receiving fingolimod therapy were recruited and fol

277 ed analysis, 13.4% and 2.9% of patients with RRMS treated and not treated with anti-CD20 had severe C

278 99 patients with NMOSD and 200 patients with RRMS were studied alongside 269 healthy controls.

279 Eligible patients with RRMS were those treated with high-efficacy MS therapy (i

280 clinical trial of HDIT/HCT for patients with RRMS who experienced relapses with loss of neurologic fu

281 All treatment-naive patients with RRMS who initiated cladribine or an S1PRM (fingolimod, o

282 Patients with RRMS with at least 1 documented relapse in the 12 months

283 In male patients with RRMS, (23)Na-MRI demonstrated a higher sodium signal in

284 Among 66 840 patients with RRMS, 1744 had used natalizumab for 6 months or longer a

285 placebo-controlled study, 249 patients with RRMS, aged 18-65 years, were eligible to be assigned equ

286 coveries on human samples from patients with RRMS, NMO, psoriasis, rheumatoid arthritis, systemic lup

287 ified an altered metabotype in patients with RRMS, represented by four changed metabolic pathways of

288 f pathogenic Th17 cytokines in patients with RRMS.

289 different leukocyte subsets of patients with RRMS.

290 phalomyelitis (EAE) but not in patients with RRMS.

291 r ongoing and future trials in patients with RRMS.

292 -1a with glatiramer acetate in patients with RRMS.

293 7F concentration in the serum of people with RRMS is associated with nonresponsiveness to therapy wit

294 27 people with RRMS, and 22 with SPMS were included in this study.

295 ononuclear cells obtained from subjects with RRMS and cell lines.

296 hibiting LAG-3 suggest that in subjects with RRMS, LAG-3 retains its ability to suppress T cell proli

297 In T cells from subjects with RRMS, we observed a global dysregulation of LAG-3 expres

298 values below the threshold, from those with RRMS (sensitivity = 90% [56 of 62], specificity = 91% [5

299 gher in patients with PMS than in those with RRMS.

300 an duration NMOSD=5.8+/-1.9 (1.9-9.9) years, RRMS=5.2+/-1.7 (1.5-9.2) years).