ライフサイエンスコーパス: experimental autoimmune

1 hrough MyD88, and subsequent amelioration of experimental autoimmune arthritis was observed to be an

2 paired autoantibody formation, and mitigates experimental autoimmune arthritis.

3 tty acids (SCFAs) have protective effects on experimental autoimmune encephalitis (EAE) responses but

4 In experimental autoimmune encephalitis (EAE), autoimmune T

5 ng a mouse model of multiple sclerosis (MS), experimental autoimmune encephalitis (EAE), we evaluated

6 f APRIL was assessed in the murine MS model, experimental autoimmune encephalitis (EAE).

7 TCH1 activation and attenuates Th17-mediated experimental autoimmune encephalitis (EAE).

8 pecific 3C-iTregs prevented the induction of experimental autoimmune encephalitis and enabled long-te

9 alleviates familial Mediterranean fever and experimental autoimmune encephalitis by targeting GSDMD.

10 nd PI3Kdelta signaling resulted in increased experimental autoimmune encephalitis disease severity.

11 with monosodium urate and the development of experimental autoimmune encephalitis in mice.

12 Experimental autoimmune encephalitis is a mouse model of

13 of STAT3 in B cells is also recapitulated in experimental autoimmune encephalitis, a mouse model of m

14 reased T-cell apoptosis, reduced severity of experimental autoimmune encephalitis, and defective immu

15 th copies of C9orf72 are more susceptible to experimental autoimmune encephalitis, mirroring the susc

16 Furthermore, in mouse experimental autoimmune encephalitis, p73-deficient mice

17 animal models of perinatal brain injury and experimental autoimmune encephalitis.

18 ived from Foxp3(lo) T(reg)P cells, prevented experimental autoimmune encephalitis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 Using experimental autoimmune encephalomyelitis (EAE) in C57BL

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

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

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

44 Following experimental autoimmune encephalomyelitis (EAE) inductio

45 Experimental autoimmune encephalomyelitis (EAE) is a mou

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

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

48 Experimental autoimmune encephalomyelitis (EAE) is the m

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

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

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

52 Using the experimental autoimmune encephalomyelitis (EAE) model of

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

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

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

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

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

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

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

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

61 Using the experimental autoimmune encephalomyelitis (EAE) model of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 Experimental autoimmune encephalomyelitis (EAE), a model

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 -12, IL-23, and p40(2) in serum of mice with experimental autoimmune encephalomyelitis (EAE), an anim

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 1 in the exacerbation of relapsing-remitting experimental autoimmune encephalomyelitis (RREAE).

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

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

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

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

169 PHTPP-mediated experimental autoimmune encephalomyelitis amelioration w

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

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

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

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

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

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

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

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

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

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

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

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

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

183 In an experimental autoimmune encephalomyelitis disease model

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

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

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

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

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

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

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

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

192 Experimental autoimmune encephalomyelitis is a CD4(+) T

193 Experimental autoimmune encephalomyelitis is a model for

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

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

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

197 In an in vivo experimental autoimmune encephalomyelitis model in which

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

199 Similarly, in experimental autoimmune encephalomyelitis model of multi

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

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

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

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

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

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

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

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

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

209 TUDCA supplementation in experimental autoimmune encephalomyelitis reduced the se

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

211 The effect on experimental autoimmune encephalomyelitis severity was M

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

213 Antibiotic treatment reduced experimental autoimmune encephalomyelitis symptoms and w

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

215 Clinical and histological experimental autoimmune encephalomyelitis was observed i

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

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

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

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

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

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

222 Here, using experimental autoimmune encephalomyelitis, an establishe

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

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

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

226 Remarkably, in experimental autoimmune encephalomyelitis, cholesterol s

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

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

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

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

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

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

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

234 In experimental autoimmune encephalomyelitis, the animal mo

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

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

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

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

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

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

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

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

243 ection and confers heightened sensitivity to experimental autoimmune encephalomyelitis.

244 cells showed impaired pathogenic function in experimental autoimmune encephalomyelitis.

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

246 lacking SLAMF9 were followed during induced experimental autoimmune encephalomyelitis.

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

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

249 increased resistance to viral infection and experimental autoimmune encephalomyelitis.

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

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

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

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

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

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

256 eficiency displayed a profound resistance to experimental autoimmune encephalomyelitis.

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

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

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

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

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

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

263 d chronic neurodegenerative phases of murine experimental autoimmune encephalomyelitis.

264 ent mice exhibited reduced susceptibility to experimental autoimmune encephalomyelitis.

265 ntiated antitumor responses, and exacerbated experimental autoimmune encephalomyelitis.

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

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

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

269 ching, protects against neuroinflammation in experimental autoimmune encephalomyelitis.

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

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

272 myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.

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

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

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

276 The murine model of MS is the experimental autoimmune encephalopathy (EAE) induced by

277 o have immunoregulatory functions in several experimental autoimmune models.

278 In this study, we used the experimental autoimmune myocarditis (EAM) model to deter

279 Inhibition of NET formation in experimental autoimmune myocarditis (EAM) of mice substa

280 t been dissected in P0106-125-induced murine experimental autoimmune neuritis.

281 in the TLR signaling pathway, was studied in experimental autoimmune neuritis.

282 g.2098 is the dominant peptide when inducing experimental autoimmune thyroiditis (EAT) in NOD mice ex

283 autoantibody production, and amelioration of experimental autoimmune thyroiditis.

284 o exhibit a massive phenotypic change during experimental autoimmune uveitis (EAU) development.

285 ow that the CD19-STAT3KO mice develop severe experimental autoimmune uveitis (EAU), an animal model o

286 Experimental autoimmune uveitis (EAU), in which CD4(+) T

287 In a rat model of experimental autoimmune uveitis (EAU), inflammation was

288 isoforms one week prior to the induction of experimental autoimmune uveitis (EAU).

289 seases such as uveitis and its animal model, experimental autoimmune uveitis (EAU).

290 nate, on uveitis using an inducible model of experimental autoimmune uveitis (EAU).

291 been shown to provide therapeutic benefit in experimental autoimmune uveitis (EAU).

292 ed the role of LXA(4) in the pathogenesis of experimental autoimmune uveitis (EAU).

293 For >30 years, the mouse model of experimental autoimmune uveitis has been employed to inv

294 dose and peptide fragments from conventional experimental autoimmune uveitis models.

295 s of IL-1R signaling confers protection from experimental autoimmune uveitis.

296 of immune cells utilizing a murine model of experimental autoimmune uveoretinitis (EAU) and the rece

297 at mesenchymal stem cells (MSCs) ameliorated experimental autoimmune uveoretinitis (EAU) in rats.

298 Experimental autoimmune uveoretinitis (EAU) is a mouse m

299 sis of the ocular infiltrate in WT mice with experimental autoimmune uveoretinitis showed a mixed pop

300 tion of pathogenic type 17 helper T cells in experimental autoimmune uveoretinitis was reduced with G