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

1 lyzed in a murine model of CNS autoimmunity (experimental autoimmune encephalomyelitis).

2 ntiated antitumor responses, and exacerbated experimental autoimmune encephalomyelitis.

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

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

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

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

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

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

9 7 cells, and consequently protects mice from experimental autoimmune encephalomyelitis.

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

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

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

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

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

15 universally required for the development of experimental autoimmune encephalomyelitis.

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

17 oxp3(+) Tregs in WT mice and amelioration of experimental autoimmune encephalomyelitis.

18 z ameliorates relapse in relapsing-remitting experimental autoimmune encephalomyelitis.

19 d macrophages, and reduces susceptibility to experimental autoimmune encephalomyelitis.

20 s Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis.

21 -lymphoid tissues and impaired resolution of experimental autoimmune encephalomyelitis.

22 ucing the clinical symptoms and pathology of experimental autoimmune encephalomyelitis.

23 Similar changes are seen in mice with experimental autoimmune encephalomyelitis.

24 sease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis.

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

26 in a skin hypersensitivity model and blocked experimental autoimmune encephalomyelitis.

27 ion in vitro, and is capable of transferring experimental autoimmune encephalomyelitis.

28 accumulation of disability and nerve loss in experimental autoimmune encephalomyelitis.

29 the presence of oxLDL induced more profound experimental autoimmune encephalomyelitis.

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

31 jugated APL at inhibiting the development of experimental autoimmune encephalomyelitis.

32 ease in a mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis.

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

34 tral protease of the coagulation cascade, in experimental autoimmune encephalomyelitis.

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

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

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

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

39 d chronic neurodegenerative phases of murine experimental autoimmune encephalomyelitis.

40 ent mice exhibited reduced susceptibility to experimental autoimmune encephalomyelitis.

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

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

43 ttenuated disease in CD4(+) T cell-dependent experimental autoimmune encephalomyelitis, a mouse model

44 d antitumor responses and reduced disease in experimental autoimmune encephalomyelitis, a mouse model

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

46 PHTPP-mediated experimental autoimmune encephalomyelitis amelioration w

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

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

49 Kv1.3-knockout (KO) mice are protected from experimental autoimmune encephalomyelitis, an animal mod

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

51 CD99 blockade in vivo ameliorated experimental autoimmune encephalomyelitis and decreased

52 X2 were partially protected from MOG-induced experimental autoimmune encephalomyelitis and displayed

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

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

55 ed arthritis were aggravated, in contrast to experimental autoimmune encephalomyelitis and immediate

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

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

58 the blood-brain barrier that occurs in both experimental autoimmune encephalomyelitis and multiple s

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

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

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

62 iRNA established protective immunity against experimental autoimmune encephalomyelitis and suppressed

63 anolipogel delivery system, markedly reduced experimental autoimmune encephalomyelitis and was 10-fol

64 sed sensitivity to septic shock, exacerbated experimental autoimmune encephalomyelitis, and a stronge

65 ecific hypersensitivity reactions, relapsing experimental autoimmune encephalomyelitis, and antibody

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

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

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

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

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

71 myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, B7-H1-Ig exhi

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

73 se results demonstrate that MEDI551 disrupts experimental autoimmune encephalomyelitis by inhibiting

74 blockers effectively reduced the severity of experimental autoimmune encephalomyelitis by suppression

75 lation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized

76 Remarkably, in experimental autoimmune encephalomyelitis, cholesterol s

77 ly improved protection from MOG35-55-induced experimental autoimmune encephalomyelitis compared with

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

79 In an experimental autoimmune encephalomyelitis disease model

80 e of MEDI551, given before or during ongoing experimental autoimmune encephalomyelitis, disrupts deve

81 which are predisposed to the development of experimental autoimmune encephalomyelitis, drastically e

82 ty, but surprisingly confers protection from experimental autoimmune encephalomyelitis (EAE) and does

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

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

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

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

87 ) of multiple sclerosis (MS) subjects and of experimental autoimmune encephalomyelitis (EAE) animals,

88 Using experimental autoimmune encephalomyelitis (EAE) as a dis

89 We used experimental autoimmune encephalomyelitis (EAE) as a mod

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

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

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

93 In an experimental autoimmune encephalomyelitis (EAE) disease

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

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

96 te Smads to inhibit Th17 differentiation and experimental autoimmune encephalomyelitis (EAE) has not

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

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

99 Using experimental autoimmune encephalomyelitis (EAE) in C57BL

100 immune-mediated inflammatory disorder model, experimental autoimmune encephalomyelitis (EAE) in commo

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

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

103 y T (Treg) cells, abrogates the induction of experimental autoimmune encephalomyelitis (EAE) in rhesu

104 a primate model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) in the c

105 Prior studies of experimental autoimmune encephalomyelitis (EAE) induced

106 Following experimental autoimmune encephalomyelitis (EAE) inductio

107 Experimental autoimmune encephalomyelitis (EAE) is a val

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

109 One hallmark of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is infil

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

111 d-Cl) on functional remyelination in chronic experimental autoimmune encephalomyelitis (EAE) mice wer

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

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

114 els in which BBB was disrupted, including an experimental autoimmune encephalomyelitis (EAE) model of

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

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

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

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

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

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

121 xN-induced model and, in the T cell-mediated experimental autoimmune encephalomyelitis (EAE) mouse mo

122 Experimental autoimmune encephalomyelitis (EAE) represen

123 T cell responses in the CxLNs and modulated experimental autoimmune encephalomyelitis (EAE) severity

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

125 e stress in multiple sclerosis (MS) plaques, experimental autoimmune encephalomyelitis (EAE) spinal c

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

127 Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was grea

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

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

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

131 lination of the CNS have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T

132 agy-related gene 7 (Atg7) in DCs ameliorated experimental autoimmune encephalomyelitis (EAE), a CD4 T

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

134 Experimental autoimmune encephalomyelitis (EAE), a model

135 letion does not benefit clinical symptoms in experimental autoimmune encephalomyelitis (EAE), a model

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

137 nervous system (CNS) of mice during chronic experimental autoimmune encephalomyelitis (EAE), a model

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

139 rine (NE) in macrophages and thereby limited experimental autoimmune encephalomyelitis (EAE), a mouse

140 and TH17 cells mediate neuroinflammation in experimental autoimmune encephalomyelitis (EAE), a mouse

141 By studying the role of IRF8 in experimental autoimmune encephalomyelitis (EAE), a mouse

142 nd that Toso(-/-) mice do not develop severe experimental autoimmune encephalomyelitis (EAE), a mouse

143 reby R-Ras contributes to autoimmunity using experimental autoimmune encephalomyelitis (EAE), a mouse

144 e immunity, NLRX1 plays a protective role in experimental autoimmune encephalomyelitis (EAE), a mouse

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

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

147 and for the initial priming of Th17 cells in experimental autoimmune encephalomyelitis (EAE), a Th17

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

149 ological correlates in Dark Agouti rats with experimental autoimmune encephalomyelitis (EAE), a widel

150 no effect on the development or severity of experimental autoimmune encephalomyelitis (EAE), althoug

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

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

153 evelopment, in adulthood, and in response to experimental autoimmune encephalomyelitis (EAE), an anim

154 helper cells (Th) during the development of experimental autoimmune encephalomyelitis (EAE), an anim

155 system demyelination and inflammation during experimental autoimmune encephalomyelitis (EAE), an anim

156 We assessed the role of HA in experimental autoimmune encephalomyelitis (EAE), an anim

157 that contributes to leukocyte trafficking in experimental autoimmune encephalomyelitis (EAE), an anim

158 pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an anim

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

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

161 of multiple sclerosis (MS), its animal model experimental autoimmune encephalomyelitis (EAE), and neu

162 nding paralysis, referred to as conventional experimental autoimmune encephalomyelitis (EAE), as oppo

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

164 d in a severe, nonresolving atypical form of experimental autoimmune encephalomyelitis (EAE), charact

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

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

167 s with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), inflamm

168 une diseases, such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), involve

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

170 multiple sclerosis (MS) and the animal model experimental autoimmune encephalomyelitis (EAE), little

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

172 short as six amino acids are therapeutic in experimental autoimmune encephalomyelitis (EAE), reducin

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

174 Experimental autoimmune encephalomyelitis (EAE), the ani

175 esent two major pathogenic T cell subsets in experimental autoimmune encephalomyelitis (EAE), the ani

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

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

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

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

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

181 on of T helper (Th) 17 cells and exacerbated experimental autoimmune encephalomyelitis (EAE), the pri

182 Toward this end, we used experimental autoimmune encephalomyelitis (EAE), the pri

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

184 During experimental autoimmune encephalomyelitis (EAE), wild-ty

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

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

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

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

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

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

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

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

193 ) attenuates chronic and relapsing-remitting experimental autoimmune encephalomyelitis (EAE).

194 clerosis (MS) and of its rodent counterpart, experimental autoimmune encephalomyelitis (EAE).

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

196 or the proinflammatory cytokine IFN-gamma in experimental autoimmune encephalomyelitis (EAE).

197 in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE).

198 s in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE).

199 of pT(reg) cells, and decreased severity of experimental autoimmune encephalomyelitis (EAE).

200 e in a neuroinflammatory autoimmunity model, experimental autoimmune encephalomyelitis (EAE).

201 n the SJL mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE).

202 immune responses and are more susceptible to experimental autoimmune encephalomyelitis (EAE).

203 n the multiple sclerosis (MS) mouse model of experimental autoimmune encephalomyelitis (EAE).

204 affected by chronic inflammation modeled by experimental autoimmune encephalomyelitis (EAE).

205 ll-mediated demyelinating autoimmune disease experimental autoimmune encephalomyelitis (EAE).

206 pathogenesis of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE).

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

208 electively enriched in the CNS tissue during experimental autoimmune encephalomyelitis (EAE).

209 tory effects in the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE).

210 x amino acids are effective therapeutics for experimental autoimmune encephalomyelitis (EAE).

211 unit of individuals with MS and of mice with experimental autoimmune encephalomyelitis (EAE).

212 (NAg) are potent, NAg-specific inhibitors of experimental autoimmune encephalomyelitis (EAE).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 nflammation and autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE); however

230 ultiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE); however

231 cause exacerbated ascending paralysis during experimental autoimmune encephalomyelitis (EAE); instead

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

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

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

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

236 cidation of factors influencing the onset of experimental autoimmune encephalomyelitis (eg, susceptib

237 in-specific Kv1.3-KO Th cells can ameliorate experimental autoimmune encephalomyelitis following tran

238 In experimental autoimmune encephalomyelitis, forced expres

239 In a mouse model of MS, experimental autoimmune encephalomyelitis, guanabenz all

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

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

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

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

244 ated T cells and shows inhibitory effects on experimental autoimmune encephalomyelitis in both preven

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

246 Moreover, experimental autoimmune encephalomyelitis in mice lackin

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

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

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

250 st the subsequent development of MOG-induced experimental autoimmune encephalomyelitis in vivo.

251 and, most importantly, in the CNS following experimental autoimmune encephalomyelitis induction, con

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

253 mmune responses and were more susceptible to experimental autoimmune encephalomyelitis induction.

254 We found that experimental autoimmune encephalomyelitis mice with an X

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

256 vous system during the inflammatory phase in experimental autoimmune encephalomyelitis mice.

257 We report that, in an MS murine model of experimental autoimmune encephalomyelitis, miR-155 contr

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 The experimental autoimmune encephalomyelitis model is a mod

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

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

265 /PD) mice were protected in a Th17-dependent experimental autoimmune encephalomyelitis model.

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

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

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

269 A new generation of spontaneous experimental autoimmune encephalomyelitis mouse models h

270 ng an increased Th17/Th1 ratio in the CNS at experimental autoimmune encephalomyelitis onset and enha

271 4 were impaired in their ability to suppress experimental autoimmune encephalomyelitis or islet allog

272 spinal cords and kidneys of mice developing experimental autoimmune encephalomyelitis or lupus, resp

273 Conversely, these mice develop severe experimental autoimmune encephalomyelitis owing to oxida

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

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

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

277 ion and the consequences of treatment in the experimental autoimmune encephalomyelitis rat model.

278 Experimental autoimmune encephalomyelitis rats were imag

279 , halofuginone shows therapeutic efficacy in experimental autoimmune encephalomyelitis, reducing both

280 , anti-SPAG16 Abs were injected in mice with experimental autoimmune encephalomyelitis, resulting in

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

282 The effect on experimental autoimmune encephalomyelitis severity was M

283 stent upregulation of SPAG16 in MS brain and experimental autoimmune encephalomyelitis spinal cord le

284 Gpr174(-/Y) mice were less susceptible to experimental autoimmune encephalomyelitis than wild-type

285 Eos(-/-) mice developed more severe experimental autoimmune encephalomyelitis than WT mice,

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

287 have previously shown in the mouse model of experimental autoimmune encephalomyelitis that transfer

288 nds (APLs), which are normally protective in experimental autoimmune encephalomyelitis, the animal mo

289 In experimental autoimmune encephalomyelitis, the animal mo

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

291 atory Th17 cells because they induced severe experimental autoimmune encephalomyelitis upon adoptive

292 Experimental autoimmune encephalomyelitis was induced by

293 Clinical and histological experimental autoimmune encephalomyelitis was observed i

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

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

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

297 ent of IFN-gamma-producing Th17 cells during experimental autoimmune encephalomyelitis, which correla

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

299 s of PTEN-targeting APCs were protected from experimental autoimmune encephalomyelitis, which was acc

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