ライフサイエンスコーパス: experimental autoimmune encephalomyelitis

1 ection and confers heightened sensitivity to experimental autoimmune encephalomyelitis.

2 increased resistance to viral infection and experimental autoimmune encephalomyelitis.

3 ed by IL-27, was unable to protect mice from experimental autoimmune encephalomyelitis.

4 and function in the steady state and during experimental autoimmune encephalomyelitis.

5 n of, and an immunotherapeutic reduction in, experimental autoimmune encephalomyelitis.

6 ed TH1 and TH17 immune responses are seen in experimental autoimmune encephalomyelitis.

7 vo, these mice exhibited reduced severity of experimental autoimmune encephalomyelitis.

8 ing multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis.

9 o differentiation and in vivo development of experimental autoimmune encephalomyelitis.

10 inflamed central nervous system of mice with experimental autoimmune encephalomyelitis.

11 eficiency displayed a profound resistance to experimental autoimmune encephalomyelitis.

12 nglion cell damage in multiple sclerosis and experimental autoimmune encephalomyelitis.

13 oils, such as collagen-induced arthritis or experimental autoimmune encephalomyelitis.

14 rd of mice subjected to chronic or relapsing experimental autoimmune encephalomyelitis.

15 d chronic neurodegenerative phases of murine experimental autoimmune encephalomyelitis.

16 LP-CD8) robustly suppress the MS mouse model experimental autoimmune encephalomyelitis.

17 ent mice exhibited reduced susceptibility to experimental autoimmune encephalomyelitis.

18 ntiated antitumor responses, and exacerbated experimental autoimmune encephalomyelitis.

19 n was increased in the murine mouse model of experimental autoimmune encephalomyelitis.

20 cell lineage, but not immunopathology during experimental autoimmune encephalomyelitis.

21 lls, present in the circulation of mice with experimental autoimmune encephalomyelitis.

22 gen receptor (ER) beta ligands could inhibit experimental autoimmune encephalomyelitis.

23 on of a T cell-dependent autoimmune disease, experimental autoimmune encephalomyelitis.

24 7 cells, and consequently protects mice from experimental autoimmune encephalomyelitis.

25 ecifically in Th17 cells protected mice from experimental autoimmune encephalomyelitis.

26 of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis.

27 cribed to develop more aggressive courses of experimental autoimmune encephalomyelitis.

28 ulatory T cells) and enhance the severity of experimental autoimmune encephalomyelitis.

29 cortical lesions, two parameters missing in experimental autoimmune encephalomyelitis.

30 universally required for the development of experimental autoimmune encephalomyelitis.

31 as wild-type littermates to T cell-dependent experimental autoimmune encephalomyelitis.

32 ching, protects against neuroinflammation in experimental autoimmune encephalomyelitis.

33 -gamma(+)CD4(+) T cells in the spleen during experimental autoimmune encephalomyelitis.

34 ls protects their axons from degeneration in experimental autoimmune encephalomyelitis.

35 myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.

36 irrored in 72 lesions from 13 marmosets with experimental autoimmune encephalomyelitis.

37 cells showed impaired pathogenic function in experimental autoimmune encephalomyelitis.

38 cell migration to the gut, also ameliorated experimental autoimmune encephalomyelitis.

39 lacking SLAMF9 were followed during induced experimental autoimmune encephalomyelitis.

40 most complete Treg-dependent protection from experimental autoimmune encephalomyelitis.

41 s in the central nervous system of mice with experimental autoimmune encephalomyelitis.

42 Further, RVX-297 prevented murine experimental autoimmune encephalomyelitis (a model of hu

43 ckade of PK renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS

44 cantly reduced throughout the progression of experimental autoimmune encephalomyelitis, a model for m

45 g MIF or D-DT developed less-severe signs of experimental autoimmune encephalomyelitis, a murine mode

46 and its administration in mice paralysed by experimental autoimmune encephalomyelitis ameliorates sy

47 PHTPP-mediated experimental autoimmune encephalomyelitis amelioration w

48 tion in delayed-type hypersensitivity and in experimental autoimmune encephalomyelitis, an animal mod

49 ng into the spinal cord of mice subjected to experimental autoimmune encephalomyelitis, an animal mod

50 Importantly, EP had in vivo impact on experimental autoimmune encephalomyelitis, an animal mod

51 L-27 efficiently prevents the development of experimental autoimmune encephalomyelitis, an autoimmune

52 Here, using experimental autoimmune encephalomyelitis, an establishe

53 fibroblastic reticular cells (FRCs), during experimental autoimmune encephalomyelitis and colitis.

54 CD99 blockade in vivo ameliorated experimental autoimmune encephalomyelitis and decreased

55 thermore, CD43(-/-) mice were protected from experimental autoimmune encephalomyelitis and had impair

56 or CaV3.1 were resistant to the induction of experimental autoimmune encephalomyelitis and had reduce

57 Mas deficiency exacerbated the course of experimental autoimmune encephalomyelitis and increased

58 al outcome in a relapsing/remitting model of experimental autoimmune encephalomyelitis and is neuropr

59 l signs and disease progression in mice with experimental autoimmune encephalomyelitis and K/BxN seru

60 of mir-181a-1/b-1 dampened the induction of experimental autoimmune encephalomyelitis and reduced ba

61 ree mice resulted in more severe symptoms of experimental autoimmune encephalomyelitis and reduced pr

62 salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensi

63 ammatory and autoimmune disorders, including experimental autoimmune encephalomyelitis and sepsis in

64 iRNA established protective immunity against experimental autoimmune encephalomyelitis and suppressed

65 we use a mouse model for multiple sclerosis, experimental autoimmune encephalomyelitis, and show that

66 mage and preserve neurologic function in the experimental autoimmune encephalomyelitis animal model o

67 players in the disease pathogenesis and the experimental autoimmune encephalomyelitis animal model.

68 ultiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinfl

69 leviate and even prevent signs of disease in experimental autoimmune encephalomyelitis, as well as ma

70 ntravenous injection of IL4I1 into mice with experimental autoimmune encephalomyelitis at disease ons

71 ublic repertoire representation in mice with experimental autoimmune encephalomyelitis at high resolu

72 acked functional synergy with MOG to promote experimental autoimmune encephalomyelitis because NFM-de

73 ective Th17 differentiation and induction of experimental autoimmune encephalomyelitis but normal thy

74 Remarkably, in experimental autoimmune encephalomyelitis, cholesterol s

75 lated immunity and protected animals against experimental autoimmune encephalomyelitis, decreasing Th

76 acking mEF-G1 in T cells were protected from experimental autoimmune encephalomyelitis, demonstrating

77 In an experimental autoimmune encephalomyelitis disease model

78 in a VEGFC - VEGFR3 dependent manner during experimental autoimmune encephalomyelitis (EAE) and drai

79 Treg cell ablation is sufficient to trigger experimental autoimmune encephalomyelitis (EAE) and faci

80 ed in-depth analysis of neurodegeneration in experimental autoimmune encephalomyelitis (EAE) and in i

81 , IFN-beta, NAg, and Alum, for inhibition of experimental autoimmune encephalomyelitis (EAE) and indu

82 t the corresponding TR1 progeny can suppress experimental autoimmune encephalomyelitis (EAE) and panc

83 a is recognized to play an important role in experimental autoimmune encephalomyelitis (EAE) and perh

84 s a critical cytokine in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and, ost

85 al programs that promote CNS inflammation in experimental autoimmune encephalomyelitis (EAE) and, pot

86 -XBP1 signaling promotes CNS inflammation in experimental autoimmune encephalomyelitis (EAE) and, pot

87 Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are infl

88 y in DCs are resistant to the development of experimental autoimmune encephalomyelitis (EAE) as a res

89 multiple sclerosis and its preclinical model experimental autoimmune encephalomyelitis (EAE) by singl

90 Resolution of established experimental autoimmune encephalomyelitis (EAE) can be a

91 w that Atxn1-null mice develop a more severe experimental autoimmune encephalomyelitis (EAE) course c

92 thogenic Th1 and Th17 responses and enhanced experimental autoimmune encephalomyelitis (EAE) developm

93 rentiation of Th17 cells in vitro and during experimental autoimmune encephalomyelitis (EAE) developm

94 aling in astrocytes reduces inflammation and experimental autoimmune encephalomyelitis (EAE) disease

95 eviously shown that loss of AMPK exacerbates experimental autoimmune encephalomyelitis (EAE) disease

96 In an experimental autoimmune encephalomyelitis (EAE) disease

97 osis triggers the development of spontaneous experimental autoimmune encephalomyelitis (EAE) during a

98 ral stem/precursor cells (NPCs) in mice with experimental autoimmune encephalomyelitis (EAE) impairs

99 of murine pathogenic TH17 cells that induce experimental autoimmune encephalomyelitis (EAE) in anima

100 Using experimental autoimmune encephalomyelitis (EAE) in C57BL

101 exaggerated T cell responses and spontaneous experimental autoimmune encephalomyelitis (EAE) in mice

102 he treatment of multiple sclerosis in man or experimental autoimmune encephalomyelitis (EAE) in mice

103 rime antigen-specific T cells and exacerbate experimental autoimmune encephalomyelitis (EAE) in mice.

104 in (Canx)-deficient mice are desensitized to experimental autoimmune encephalomyelitis (EAE) inductio

105 Following experimental autoimmune encephalomyelitis (EAE) inductio

106 Experimental autoimmune encephalomyelitis (EAE) is a mou

107 sly, we showed that the sexual dimorphism in experimental autoimmune encephalomyelitis (EAE) is assoc

108 he function of B cells in the MS mouse model experimental autoimmune encephalomyelitis (EAE) is large

109 ch as multiple sclerosis and its mouse model experimental autoimmune encephalomyelitis (EAE) is tempo

110 Experimental autoimmune encephalomyelitis (EAE) is the m

111 TLR signaling in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is uncle

112 ll as PLP138-151-induced relapsing-remitting experimental autoimmune encephalomyelitis (EAE) mice.

113 We first employed the experimental autoimmune encephalomyelitis (EAE) model an

114 strocyte-specific transcriptome in ON in the experimental autoimmune encephalomyelitis (EAE) model of

115 of feces harvested at peak disease from the experimental autoimmune encephalomyelitis (EAE) model of

116 y in a rat model of arthritis and in a mouse experimental autoimmune encephalomyelitis (EAE) model of

117 reconditioning suppresses development of the experimental autoimmune encephalomyelitis (EAE) model of

118 oligodendrocytes against inflammation in the experimental autoimmune encephalomyelitis (EAE) model of

119 cells failed to fully develop disease in the experimental autoimmune encephalomyelitis (EAE) model of

120 of Th17 cells in vitro and in vivo using the experimental autoimmune encephalomyelitis (EAE) model of

121 y, and occurs in both MS patients and in the experimental autoimmune encephalomyelitis (EAE) model of

122 Using the experimental autoimmune encephalomyelitis (EAE) model of

123 Using the experimental autoimmune encephalomyelitis (EAE) model of

124 Using the experimental autoimmune encephalomyelitis (EAE) model, w

125 yzed the respective animals in vivo using an experimental autoimmune encephalomyelitis (EAE) model.

126 in driving chronic pain in MS using a mouse experimental autoimmune encephalomyelitis (EAE) model.

127 pact of Notch signaling in macrophages in an experimental autoimmune encephalomyelitis (EAE) model.

128 We used the experimental autoimmune encephalomyelitis (EAE) models i

129 e severe inflammatory disease in colitis and experimental autoimmune encephalomyelitis (EAE) models.

130 , notably in multiple sclerosis (MS) and its experimental autoimmune encephalomyelitis (EAE) models.

131 HA synthesis, on disease progression in the experimental autoimmune encephalomyelitis (EAE) mouse mo

132 on multiple sclerosis development, using the experimental autoimmune encephalomyelitis (EAE) mouse mo

133 y Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse mo

134 We find that some PC in the CNS of mice with experimental autoimmune encephalomyelitis (EAE) originat

135 presentation during MS and its animal model experimental autoimmune encephalomyelitis (EAE) remain u

136 of the protein kinase CK2 (CK2) ameliorates experimental autoimmune encephalomyelitis (EAE) severity

137 n oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using Ah

138 e (CLP)-induced sepsis on the development of experimental autoimmune encephalomyelitis (EAE) was expl

139 To model CNS infiltration by B cells, experimental autoimmune encephalomyelitis (EAE) was indu

140 Disease severity of experimental autoimmune encephalomyelitis (EAE) was sign

141 d a comorbid model system in which mice with experimental autoimmune encephalomyelitis (EAE) were adm

142 We tested this using a model of experimental autoimmune encephalomyelitis (EAE) with hip

143 h nodes isolated during the priming phase of experimental autoimmune encephalomyelitis (EAE), a CD4(+

144 ction in vivo and attenuated the severity of experimental autoimmune encephalomyelitis (EAE), a disea

145 Experimental autoimmune encephalomyelitis (EAE), a model

146 ats, vitamin D supplementation protects from experimental autoimmune encephalomyelitis (EAE), a model

147 Experimental autoimmune encephalomyelitis (EAE), a model

148 ported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse

149 the transcription factor Bhlhe40 to mediate experimental autoimmune encephalomyelitis (EAE), a mouse

150 We examined CD48 expression and function in experimental autoimmune encephalomyelitis (EAE), a mouse

151 ucts (FHES) attenuated the clinical signs of experimental autoimmune encephalomyelitis (EAE), a mouse

152 ssary for pathogenic Th17 cell generation in experimental autoimmune encephalomyelitis (EAE), a mouse

153 In female mice with experimental autoimmune encephalomyelitis (EAE), a murin

154 itic cells and suppressed the development of experimental autoimmune encephalomyelitis (EAE), a precl

155 UV light suppresses experimental autoimmune encephalomyelitis (EAE), a widel

156 filtrating the central nervous system during experimental autoimmune encephalomyelitis (EAE), a widel

157 iR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an anim

158 nges to the gut microbiome that occur during experimental autoimmune encephalomyelitis (EAE), an anim

159 PCs) within the spinal cord leptomeninges in experimental autoimmune encephalomyelitis (EAE), an anim

160 derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an anim

161 R knockout mice had more disease severity in experimental autoimmune encephalomyelitis (EAE), an anim

162 lay an important role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an anim

163 the effects and mechanism of action of Ba in experimental autoimmune encephalomyelitis (EAE), an anim

164 -12, IL-23, and p40(2) in serum of mice with experimental autoimmune encephalomyelitis (EAE), an anim

165 lammatory, and neuroprotective properties in experimental autoimmune encephalomyelitis (EAE), an anim

166 as been shown by our laboratory to attenuate experimental autoimmune encephalomyelitis (EAE), an anim

167 ory disorders, such as multiple sclerosis or experimental autoimmune encephalomyelitis (EAE), an esta

168 nces in the astrocyte transcriptome occur in experimental autoimmune encephalomyelitis (EAE), an MS m

169 L2 were effective in suppressing MOG-induced experimental autoimmune encephalomyelitis (EAE), and the

170 ts a role for IL-1 in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), but how

171 on partially and inhibits the development of experimental autoimmune encephalomyelitis (EAE), deletio

172 , because the most widely used animal model, experimental autoimmune encephalomyelitis (EAE), does no

173 ase multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), expansi

174 on and immune-mediated demyelination through experimental autoimmune encephalomyelitis (EAE), have pr

175 PPAR-delta develop an exacerbated course of experimental autoimmune encephalomyelitis (EAE), highlig

176 Its corresponding animal model, experimental autoimmune encephalomyelitis (EAE), is wide

177 ion of RORgammat prevents TH17 cell-mediated experimental autoimmune encephalomyelitis (EAE), it also

178 ease of the CNS, and in its mouse model, the experimental autoimmune encephalomyelitis (EAE), miRNA d

179 venously for 6 consecutive days to mice with experimental autoimmune encephalomyelitis (EAE), PLG-H p

180 focus of MS research using the animal model experimental autoimmune encephalomyelitis (EAE), substan

181 c GR deletion in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the ani

182 tiation 4-positive (CD4(+)) T cells promotes experimental autoimmune encephalomyelitis (EAE), the ani

183 Experimental autoimmune encephalomyelitis (EAE), the ani

184 In both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), the C-C

185 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), the mec

186 ht to determine the specific role of TSPO in experimental autoimmune encephalomyelitis (EAE), the mos

187 n anti-CD19 mAb, therapeutically ameliorates experimental autoimmune encephalomyelitis (EAE), the mou

188 be refractory to recovery from the signs of experimental autoimmune encephalomyelitis (EAE), the mou

189 We used a murine model of MS, experimental autoimmune encephalomyelitis (EAE), to eval

190 ilized the principal autoimmune model of MS, experimental autoimmune encephalomyelitis (EAE), togethe

191 BM components, laminin 411 or 511, in murine experimental autoimmune encephalomyelitis (EAE), we show

192 Using an animal model of MS, experimental autoimmune encephalomyelitis (EAE), we show

193 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), we used

194 n oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE).

195 induced in a subset of effector CD4 cells in experimental autoimmune encephalomyelitis (EAE).

196 yelin debris in spinal cord injury (SCI) and experimental autoimmune encephalomyelitis (EAE).

197 odel system of autoimmune neuroinflammation, experimental autoimmune encephalomyelitis (EAE).

198 autoimmunity in mouse models of colitis and experimental autoimmune encephalomyelitis (EAE).

199 godendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis (EAE).

200 and their disease-modulating activity on the Experimental Autoimmune Encephalomyelitis (EAE).

201 ltiple sclerosis (MS) and of its mouse model experimental autoimmune encephalomyelitis (EAE).

202 d with a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE).

203 M-SOB on susceptibility of C57BL/6J mice to experimental autoimmune encephalomyelitis (EAE).

204 ding multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE).

205 f S1P1 in Th17 cells conferred resistance to experimental autoimmune encephalomyelitis (EAE).

206 and can also suppress the manifestations of experimental autoimmune encephalomyelitis (EAE).

207 nflammation, such as the spinal cord, during experimental autoimmune encephalomyelitis (EAE).

208 astrocytes in the most widely used MS model, experimental autoimmune encephalomyelitis (EAE).

209 o create effective ASIT for the treatment of experimental autoimmune encephalomyelitis (EAE).

210 l cells in both human MS and the mouse model experimental autoimmune encephalomyelitis (EAE).

211 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).

212 t of multiple sclerosis in a murine model of experimental autoimmune encephalomyelitis (EAE).

213 cells during autoimmune responses, including experimental autoimmune encephalomyelitis (EAE).

214 G peptide resulted in attenuated severity of experimental autoimmune encephalomyelitis (EAE).

215 as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE).

216 in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE).

217 ide [T20K]kalata B1 using the MS mouse model experimental autoimmune encephalomyelitis (EAE).

218 bates the clinical phenotype of the MS model experimental autoimmune encephalomyelitis (EAE).

219 ey mediator of tmTNF-dependent protection in experimental autoimmune encephalomyelitis (EAE).

220 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).

221 suppress progression of relapsing-remitting experimental autoimmune encephalomyelitis (EAE).

222 rine Th1 cell- and Th17 cell-driven model of experimental autoimmune encephalomyelitis (EAE).

223 central nervous system (CNS) inflammation in experimental autoimmune encephalomyelitis (EAE).

224 on of Nrf2 in DMF treatment of the MS model, experimental autoimmune encephalomyelitis (EAE).

225 n the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).

226 ion, neuroinflammation, and demyelination in experimental autoimmune encephalomyelitis (EAE).

227 monstrated that DHH is down-regulated during experimental autoimmune encephalomyelitis (EAE).

228 entiation and protected mice from developing experimental autoimmune encephalomyelitis (EAE).

229 ays the onset and impedes the progression of experimental autoimmune encephalomyelitis (EAE).

230 lodynia and facial grimacing in animals with experimental autoimmune encephalomyelitis (EAE).

231 ssic CD4+ T cell-mediated autoimmune disease experimental autoimmune encephalomyelitis (EAE).

232 in, and in inflammatory brain lesions during experimental autoimmune encephalomyelitis (EAE).

233 quired for maximal clinical and histological experimental autoimmune encephalomyelitis (EAE); and ide

234 multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE); however

235 utoimmune cells that attack myelin sheath in experimental autoimmune encephalomyelitis (EAE, an anima

236 sue during neuroinflammation associated with experimental autoimmune encephalomyelitis (EAE; a mouse

237 Acute loss of function in an MS model (experimental autoimmune encephalomyelitis [EAE]) is part

238 an experimental model of multiple sclerosis [experimental autoimmune encephalomyelitis, (EAE)] and a

239 rosis (MS) and a mouse model of the disease (experimental autoimmune encephalomyelitis; EAE), but the

240 alpha fused to apolipoprotein A-1 vectors in experimental autoimmune encephalomyelitis, even at low d

241 mechanism of immune-mediated inflammation in experimental autoimmune encephalomyelitis has been exten

242 otective effects in autoimmune diseases like experimental autoimmune encephalomyelitis; however, its

243 When subjected to experimental autoimmune encephalomyelitis, IL-17R-signal

244 cumulated less efficiently in the CNS during experimental autoimmune encephalomyelitis in a competiti

245 GOT1 with (aminooxy)acetic acid ameliorated experimental autoimmune encephalomyelitis in a therapeut

246 to bisphenol-A increased the development of experimental autoimmune encephalomyelitis in adulthood i

247 sing the susceptibility of the recipients to experimental autoimmune encephalomyelitis in an IL-1 rec

248 Treatment with ACs reduces the severity of experimental autoimmune encephalomyelitis in hosts with

249 , and in addition, inhibition of GSK3 limits experimental autoimmune encephalomyelitis in mice.

250 duction in vitro and in vivo and ameliorates experimental autoimmune encephalomyelitis in mice.

251 mod (FTY720) ameliorated chronic progressive experimental autoimmune encephalomyelitis in nonobese di

252 in vivo during antigen-induced arthritis and experimental autoimmune encephalomyelitis, indicating th

253 mer-positive T cells and promoted consistent experimental autoimmune encephalomyelitis induction, unl

254 Experimental autoimmune encephalomyelitis is a CD4(+) T

255 Experimental autoimmune encephalomyelitis is a model for

256 nation of the brain in a clinically-relevant experimental autoimmune encephalomyelitis mice model.

257 ) T cells and monocytes expressed ANKRD55 in experimental autoimmune encephalomyelitis mice, with the

258 adjuvant arthritis model (AA) and the mouse experimental autoimmune encephalomyelitis model (EAE).

259 In an in vivo experimental autoimmune encephalomyelitis model in which

260 es clinical disease when administered in the experimental autoimmune encephalomyelitis model of MS.

261 Similarly, in experimental autoimmune encephalomyelitis model of multi

262 We reported in a nonhuman primate experimental autoimmune encephalomyelitis model that an

263 ious in reducing disease severity in a mouse experimental autoimmune encephalomyelitis model, demonst

264 encephalitogenic function of T cells in the experimental autoimmune encephalomyelitis model.

265 red after priming using an adoptive transfer experimental autoimmune encephalomyelitis model.

266 e role of EVs from blood plasma (pEVs) in an experimental autoimmune encephalomyelitis mouse model of

267 iR-27a-3p, are upregulated in neurons in the experimental autoimmune encephalomyelitis mouse model of

268 f the two drugs at the peak of disease in an experimental autoimmune encephalomyelitis mouse model of

269 t they express LAG3 in the late phase in the experimental autoimmune encephalomyelitis mouse model of

270 cytes leads to phenotypes reminiscent of the experimental autoimmune encephalomyelitis mouse model wi

271 led to exacerbated neuroinflammation in the experimental autoimmune encephalomyelitis mouse model.

272 lls were resistant to an autoimmune disease, experimental autoimmune encephalomyelitis, often mediate

273 4 were impaired in their ability to suppress experimental autoimmune encephalomyelitis or islet allog

274 vivo, RGC-32(-/-) mice display an attenuated experimental autoimmune encephalomyelitis phenotype acco

275 nt mice presented with a similar ameliorated experimental autoimmune encephalomyelitis phenotype as S

276 rmatitis, and were resistant to induction of experimental autoimmune encephalomyelitis, presumably by

277 ysolecithin-induced demyelination as well as experimental autoimmune encephalomyelitis, principal ani

278 TUDCA supplementation in experimental autoimmune encephalomyelitis reduced the se

279 1 in the exacerbation of relapsing-remitting experimental autoimmune encephalomyelitis (RREAE).

280 We show in this article that TSSP increases experimental autoimmune encephalomyelitis severity by li

281 The effect on experimental autoimmune encephalomyelitis severity was M

282 plenic Th17 cell differentiation and reduced experimental autoimmune encephalomyelitis severity.

283 the resulting progeny developed spontaneous experimental autoimmune encephalomyelitis (spEAE), which

284 Antibiotic treatment reduced experimental autoimmune encephalomyelitis symptoms and w

285 pectrum disorder (NMOSD) and in TH17-induced experimental autoimmune encephalomyelitis (TH17-EAE).

286 icantly reduced active and adoptive-transfer experimental autoimmune encephalomyelitis that is charac

287 In experimental autoimmune encephalomyelitis, the animal mo

288 It has been demonstrated that during experimental autoimmune encephalomyelitis there are myel

289 In adult marmosets with experimental autoimmune encephalomyelitis, vessel-wall f

290 Clinical and histological experimental autoimmune encephalomyelitis was observed i

291 y using a mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis, we demonstrat

292 Using a murine model of multiple sclerosis, experimental autoimmune encephalomyelitis, we demonstrat

293 ma T cell line derived from a mouse model of experimental autoimmune encephalomyelitis, we observed t

294 In stark contrast, using experimental autoimmune encephalomyelitis, we show that

295 nt autoimmune diseases such as arthritis and experimental autoimmune encephalomyelitis, where c-Rel p

296 it lesions in rhesus monkey brain induced by experimental autoimmune encephalomyelitis, which is the

297 MOG(35-55) peptide, resulting in less severe experimental autoimmune encephalomyelitis, which was ass

298 mentation reduced the severity of subsequent experimental autoimmune encephalomyelitis, which was ass

299 ne Th1 and Th17 cells independently transfer experimental autoimmune encephalomyelitis (widely used a

300 levels above 200 nmol/l developed fulminant experimental autoimmune encephalomyelitis with massive C