ライフサイエンスコーパス: EAE

1 EAE mice accumulate (18)F-FAC in the brain at 180% of th

2 EAE suppression was associated with the expansion of MOG

3 isocaloric diet for 3 wk prior to MOG(35-55) EAE induction.

4 n peripheral myeloid lineage cells abrogated EAE, which was associated with decreased antigen-specifi

5 late antigen-4 (VLA-4) deficiency abrogated EAE dependent on B cell antigen presentation.

6 ells whose presence were required to achieve EAE recovery.

7 enuated EAE disease severity and ameliorated EAE-induced oligodendrocyte loss, demyelination, and axo

8 nse of WT Th17 cells and thereby ameliorated EAE.

9 rocyte pathogenic activities and ameliorates EAE.

10 Synthetic miR-30d given orally ameliorates EAE through expansion of regulatory T cells (Tregs).

11 eared the brain of T-cell infiltration in an EAE mouse model of multiple sclerosis (MS).

12 , in mice having both liver autoimmunity and EAE, liver inflammation sequestered these ubiquitous or

13 tivity and promotes Th17 differentiation and EAE.

14 w the latent period between immunization and EAE's overt symptom onset is characterized by distinct h

15 intact spinal cord in both lysolecithin- and EAE-mediated demyelination models.

16 MS and EAE are characterized by inflammation, demyelination, an

17 paB activation in oligodendrocytes in MS and EAE remains elusive.

18 optic nerve condition that occurs in MS and EAE.

19 ERK activation on oligodendrocytes in MS and EAE.SIGNIFICANCE STATEMENT Nuclear factor kappaB (NF-kap

20 NF-kappaB plays a critical role in MS and EAE; however, the effects of NF-kappaB activation on oli

21 ic angiogenesis and fibrosis in both SCI and EAE.

22 ressurized liquid (PLE) and enzyme assisted (EAE) extractions.

23 DGAT1 inhibition or deficiency attenuated EAE, with associated enhanced Treg frequency; and enceph

24 aB activation in oligodendrocytes attenuated EAE disease severity and ameliorated EAE-induced oligode

25 Vancomycin administration attenuated both EAE symptoms and protease inhibitor induction potentiall

26 e therapy also reduces demyelination in both EAE and a model of the early MS lesion.

27 changes of the TCRbeta repertoire driven by EAE and pregnancy using TCR sequencing.

28 elitis (EAE), and they downregulated chronic EAE.

29 In mice with chronic EAE, SA-IL-4 inhibits immune-cell infiltration into the

30 e on T cells in the CNS ameliorated clinical EAE symptoms.

31 ion of B(regs) reverses established clinical EAE and that clinical improvement is associated with a s

32 uperior to Tecfidera in suppressing clinical EAE.

33 eces from naive mice and those exhibiting CP-EAE or RR-EAE revealed significantly diverse microbial p

34 stablish a novel, efficient B cell-dependent EAE model.

35 representing the most-used B cell-dependent EAE model.

36 ells was reduced, and the autoimmune disease EAE was exacerbated in mice.

37 the expansion of Treg harboring the dominant EAE-associated TRBV13-2 chain and increased the frequenc

38 vement of PPAR-delta in myeloid cells during EAE using mice that had Cre-mediated excision of floxed

39 commensal Lactobacillaceae decreases during EAE while other commensal populations belonging to the C

40 C are dramatically reduced in the gut during EAE, and likewise, a reduction in IgA-bound fecal bacter

41 in ON astrocytes at the protein level during EAE.

42 l ganglion cell (RGC) and axonal loss during EAE optic neuritis.

43 tics do not undergo lymphangiogenesis during EAE, suggesting heterogeneity in CNS lymphatics.

44 iferation in the draining lymph nodes during EAE.

45 f PERK activation on oligodendrocytes during EAE are not mediated by activating transcription factor

46 lta in DC in limiting Th cell priming during EAE.

47 beta-catenin signaling in CNS vessels during EAE/MS partially restores functional BBB integrity and l

48 cores in experimental allergic encephalitis (EAE) and in the cuprizone model of demyelination/remyeli

49 cts on experimental autoimmune encephalitis (EAE) responses but the detailed roles of SCFAs and their

50 (MS), experimental autoimmune encephalitis (EAE), we evaluated the role of gut microbiota in modulat

51 model, experimental autoimmune encephalitis (EAE).

52 in experimental allergic encephalomyelitis (EAE), a murine model of multiple sclerosis.

53 g experimental autoimmune encephalomyelitis (EAE) and drain both CSF and cells that were once in the

54 r experimental autoimmune encephalomyelitis (EAE) and facial allodynia in immunized female mice.

55 s experimental autoimmune encephalomyelitis (EAE) and pancreatic beta cell autoreactivity.

56 f experimental autoimmune encephalomyelitis (EAE) and, ostensibly, in multiple sclerosis.

57 n experimental autoimmune encephalomyelitis (EAE) and, potentially, MS.

58 n experimental autoimmune encephalomyelitis (EAE) and, potentially, multiple sclerosis.

59 d experimental autoimmune encephalomyelitis (EAE) are inflammatory diseases of the CNS in which Th17

60 l experimental autoimmune encephalomyelitis (EAE) by single-cell RNA sequencing in combination with c

61 e experimental autoimmune encephalomyelitis (EAE) course compared to wildtype mice.

62 d experimental autoimmune encephalomyelitis (EAE) development.

63 g experimental autoimmune encephalomyelitis (EAE) development.

64 s experimental autoimmune encephalomyelitis (EAE) during adolescence and early young adulthood, while

65 h experimental autoimmune encephalomyelitis (EAE) impairs the accumulation of inflammatory monocyte-d

66 r experimental autoimmune encephalomyelitis (EAE) in mice [poly(Y,E,A,K)(n), known as Copaxone, and p

67 o experimental autoimmune encephalomyelitis (EAE) induction, a model that is frequently used to study

68 Experimental autoimmune encephalomyelitis (EAE) is a mouse disease model with brain-infiltrating le

69 l experimental autoimmune encephalomyelitis (EAE) is largely confined to induction with either the my

70 l experimental autoimmune encephalomyelitis (EAE) is temporarily suppressed by pregnancy.

71 Experimental autoimmune encephalomyelitis (EAE) is the most common model of multiple sclerosis (MS)

72 g experimental autoimmune encephalomyelitis (EAE) mice.

73 e experimental autoimmune encephalomyelitis (EAE) model and observed pronounced immunomodulation evid

74 e experimental autoimmune encephalomyelitis (EAE) model of MS ameliorates disease in recipients in a

75 e experimental autoimmune encephalomyelitis (EAE) model of MS, we determined that macrophages within

76 e experimental autoimmune encephalomyelitis (EAE) model of MS, which recapitulates CD4+ T cell-depend

77 e experimental autoimmune encephalomyelitis (EAE) model of MS.

78 e experimental autoimmune encephalomyelitis (EAE) model of MS.

79 e experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS), no one has yet ex

80 e experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS).

81 e experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis.

82 e experimental autoimmune encephalomyelitis (EAE) model of Th17 cell-driven pathology.

83 n experimental autoimmune encephalomyelitis (EAE) model.

84 d experimental autoimmune encephalomyelitis (EAE) models.

85 s experimental autoimmune encephalomyelitis (EAE) models.

86 n experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced di

87 h experimental autoimmune encephalomyelitis (EAE) originate in the gut and produce immunoglobulin A (

88 l experimental autoimmune encephalomyelitis (EAE) remain undefined.

89 f experimental autoimmune encephalomyelitis (EAE) was explored.

90 , experimental autoimmune encephalomyelitis (EAE) was induced in transgenic mice that express human C

91 f experimental autoimmune encephalomyelitis (EAE) was significantly exacerbated in Iqgap1(-/-) mice a

92 f experimental autoimmune encephalomyelitis (EAE), a CD4(+) T cell-driven mouse model of multiple scl

93 Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, exhibits such dise

94 n experimental autoimmune encephalomyelitis (EAE), a mouse model for human multiple sclerosis.

95 f experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS).

96 h experimental autoimmune encephalomyelitis (EAE), a murine model of MS, adoptive transfer of IL-10(+

97 f experimental autoimmune encephalomyelitis (EAE), a preclinical model of MS, in preventive and thera

98 g experimental autoimmune encephalomyelitis (EAE), a widely studied animal model of MS, expressed hig

99 s experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS, in mice and may

100 g experimental autoimmune encephalomyelitis (EAE), an animal model for MS.

101 e experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS).

102 h experimental autoimmune encephalomyelitis (EAE), an animal model of MS, as compared to control mice

103 n experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

104 e experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

105 f experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

106 n experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis.

107 r experimental autoimmune encephalomyelitis (EAE), an established mouse model mimicking part of the h

108 n experimental autoimmune encephalomyelitis (EAE), an MS model.

109 d experimental autoimmune encephalomyelitis (EAE), and they downregulated chronic EAE.

110 , experimental autoimmune encephalomyelitis (EAE), does not present this aspect of the disease.

111 h experimental autoimmune encephalomyelitis (EAE), have provided valuable insights into the mechanism

112 f experimental autoimmune encephalomyelitis (EAE), highlighting a role for this nuclear receptor in l

113 , experimental autoimmune encephalomyelitis (EAE), is widely used to understand disease pathogenesis

114 d experimental autoimmune encephalomyelitis (EAE), it also disrupts thymocyte development, which coul

115 h experimental autoimmune encephalomyelitis (EAE), PLG-H particles had significantly lower EAE clinic

116 l experimental autoimmune encephalomyelitis (EAE), substantial evidence from patients with MS points

117 g experimental autoimmune encephalomyelitis (EAE), the animal model of MS, resulted in a reduced Treg

118 f experimental autoimmune encephalomyelitis (EAE), the mouse model of multiple sclerosis.

119 , experimental autoimmune encephalomyelitis (EAE), to evaluate the hypothesis that the loss of plasmi

120 , experimental autoimmune encephalomyelitis (EAE), together with a genetically diverse mouse model re

121 , experimental autoimmune encephalomyelitis (EAE), we show here that injection of anti-hnRNP A1 antib

122 e experimental autoimmune encephalomyelitis (EAE), we show here that loss of endothelial laminin 511

123 , experimental autoimmune encephalomyelitis (EAE), we used intravital microscopy, assessing local cel

124 g experimental autoimmune encephalomyelitis (EAE).

125 f experimental autoimmune encephalomyelitis (EAE).

126 h experimental autoimmune encephalomyelitis (EAE).

127 e experimental autoimmune encephalomyelitis (EAE).

128 g experimental autoimmune encephalomyelitis (EAE).

129 d experimental autoimmune encephalomyelitis (EAE).

130 n experimental autoimmune encephalomyelitis (EAE).

131 d experimental autoimmune encephalomyelitis (EAE).

132 , experimental autoimmune encephalomyelitis (EAE).

133 d experimental autoimmune encephalomyelitis (EAE).

134 d experimental autoimmune encephalomyelitis (EAE).

135 f experimental autoimmune encephalomyelitis (EAE).

136 , experimental autoimmune encephalomyelitis (EAE).

137 n experimental autoimmune encephalomyelitis (EAE).

138 g experimental autoimmune encephalomyelitis (EAE).

139 l experimental autoimmune encephalomyelitis (EAE); and identified CMKLR1 small molecule antagonist 2-

140 l experimental autoimmune encephalomyelitis (EAE); however, the role of NF-kappaB activation in oligo

141 (experimental autoimmune encephalomyelitis [EAE]) is partly due to central nervous system (CNS) hypo

142 the experimental autoimmune encephalopathy (EAE) induced by immunization of mice with myelin oligode

143 Moreover, mtROS blockade during established EAE markedly ameliorates disease severity, dampening aut

144 AE disease progression and helps to evaluate EAE as a viable model for gut dysbiosis in MS patients.

145 GM-CSF production by T cells and exacerbated EAE upon adoptive transfer than did wild-type DCs.

146 mablast (PB) plus PC resulted in exacerbated EAE that was normalized by the introduction of gut-deriv

147 ized B cell-deficient mice failed to exhibit EAE.

148 However, contrary to initial expectations, EAE-challenged plasminogen-deficient (Plg(-)) mice devel

149 Embryonic alcohol exposure (EAE) in male zebrafish increased the propensity for diet

150 evelopment of an enzyme-assisted extraction (EAE) method to obtain NEPs from sweet cherry pomace empl

151 iquid (PLE) and enzyme-assisted extractions (EAE).

152 immune cells and is also a prerequisite for EAE pathogenesis.

153 transcriptome analysis in CD4+ T cells from EAE mice with a specific deletion of Kdm6a showed upregu

154 APRIL was expressed in lesions from EAE.

155 In mice having EAE, nanomedicines displaying either ubiquitous or CNS-s

156 D4(+) T cells exhibited significantly higher EAE scores than those with their wild-type counterparts,

157 ake in the brain and spinal cord of huCD20tg EAE, and B220 immunostaining verified that increased (64

158 in epitope (PLP(178-191)) elicited identical EAE in WT and muMT mice, suggesting an absence of B cell

159 In EAE and in the cuprizone model, areas of myelin loss, wh

160 In EAE, improvement in paralytic scores was seen when the d

161 In EAE, remyelination was induced with estrogen receptor-be

162 In EAE-induced female mice, adoptive transfer of Treg cells

163 upregulated in the CSF of MS patients and in EAE cerebellum.

164 We identified astrocytes in EAE and multiple sclerosis that were characterized by de

165 pathways, respectively, in ON astrocytes in EAE.

166 ting a role for gut microbial composition in EAE pathogenesis.

167 G)35-55 The mechanism of action of GM-CSF in EAE is poorly understood.

168 oss of function in EAE, and demyelination in EAE, and the model of the early MS lesion, seem to be du

169 iscovery that NAS neuroprotective effects in EAE are abrogated in mice lacking IDO1 expression, we in

170 d MS drug Tecfidera for clinical efficacy in EAE; characterized key safety/toxicity parameters for al

171 in C3 expressing ON astrocytes was found in EAE females versus healthy females, as compared to that

172 Loss of function in EAE, and demyelination in EAE, and the model of the earl

173 ression, to pathogenic Th17 cell function in EAE.

174 cord PET signal was significantly higher in EAE mice than in controls at all evaluated time points (

175 We report that the tissue hypoxia in EAE is associated with a profound hypoperfusion of the i

176 vidence of proteases and their inhibitors in EAE and highlight the utility stool-omics for revealing

177 tinal ganglion cell (RGC) and axonal loss in EAE females.

178 nRNP A1, play a role in neurodegeneration in EAE with important implications for the pathogenesis of

179 Though axon injury occurs in EAE, it is rapid and acute, making it difficult to inter

180 of PERK inactivation in oligodendrocytes in EAE were accompanied by impaired NF-kappaB activation in

181 tanding of the mechanisms underlying pain in EAE and suggest potential treatment strategies for pain

182 al modules, contributing to CNS pathology in EAE and, potentially, multiple sclerosis.

183 ochondrial function, and tissue perfusion in EAE.

184 er 17 cells, a pathogenic cell population in EAE.

185 several Firmicutes known to be protective in EAE.

186 le mice to study the role of this protein in EAE.

187 eloid cells exhibited a drastic reduction in EAE incidence.

188 S is a method to measure disease severity in EAE without subjective bias and is a tool to consistentl

189 L-1beta- and GLAST-dependent synaptopathy in EAE wild-type mice.

190 rsus healthy females, as compared to that in EAE males versus healthy males.

191 sponsible for the protective action of UV in EAE and presumably human MS.

192 ssing local cellular interactions in vivo in EAE animals and ex vivo in organotypic hippocampal slice

193 Furthermore, immunization to induce EAE led to significant alterations in gut microbiota, so

194 In contrast, PLP(ECD) induced EAE not only in WT mice, but in B cell-sufficient mice i

195 Inducing EAE by immunization with a myelin oligodendrocyte glycop

196 Gut microbes also influence EAE severity, yet their impact on the latent period rema

197 ited to the CNS during CD4+ T cell-initiated EAE engaged in determinant spreading and influenced dise

198 nted in the CNS during CD4+ T cell-initiated EAE.

199 eneration in anti-hnRNP A1 antibody injected EAE mice.

200 Tgfb2-/- NPCs transplanted into EAE mice were ineffective in impairing MC accumulation w

201 ccumulates in brain-infiltrating leukocytes, EAE mice were analyzed with (18)F-FAC PET, digital autor

202 Hectd3-deficient mice have lower EAE severity, reduced Th17 program and inefficient Th17

203 AE), PLG-H particles had significantly lower EAE clinical scores than PBS control, while PLG-L and PD

204 we found that the expression pattern of many EAE-induced genes was reversed by CBD treatment which wa

205 These findings suggest that mild EAE coupled with natural aging may be a solution to bett

206 y identical hosts was sufficient to modulate EAE susceptibility and systemic metabolite profiles.

207 is study, we investigated how IL-9 modulates EAE development.

208 d H3K27me3 marks in CD4+ T cells from naive, EAE and CBD treated EAE mice by ChIP-seq.

209 Using a new EAE system that incorporates temporal regulation of MHCI

210 Amelioration of EAE via GlcNAc treatment suggests a novel first-defense

211 We identified several consequences of EAE that may contribute to these phenotypes, including a

212 activity of triterpenoids in the context of EAE.

213 We further observed in the spinal cords of EAE B(regs)-treated mice that CNS resident CD11b/CD45(in

214 ltration into the brains and spinal cords of EAE mice.

215 that are occurring throughout the course of EAE disease progression and helps to evaluate EAE as a v

216 We hypothesized that clinical courses of EAE may be shaped by differential gut microbiota.

217 unexpectedly associated with exacerbation of EAE in a genetically susceptible host, which was functio

218 ally abundant bacteria in CP and RR forms of EAE, indicating a potential role for gut microbiota in s

219 mine the susceptibility to CP or RR forms of EAE.

220 RBV13-2 chain and increased the frequency of EAE-associated clonotypes within the Treg compartment.

221 o-polarized Th17 cells were poor inducers of EAE in adoptive recipients.

222 these Tregs were protected from induction of EAE by the appropriate autoantigen.

223 togenic T cells and promote the induction of EAE during the age window of young adulthood.

224 ical and neuropathological manifestations of EAE disappeared in miR-142 knock-out mice.

225 vents, we studied a T-cell-mediated model of EAE combining in vivo two-photon microscopy with two dif

226 ns in the SJL/J-relapsing-remitting model of EAE, and could comparably assess the therapeutic efficie

227 Using a relapsing-remitting model of EAE, here we demonstrate that when applied to preexistin

228 The modulation of EAE by CCL2 was associated with downregulation of Th1/Th

229 he relevance of Kdm6a in the pathogenesis of EAE as a model of MS.

230 clinical symptoms and disease progression of EAE.

231 e decline in both progression and relapse of EAE occurred as a result of reduced demyelination and my

232 that silencing Chi3l3 increases severity of EAE.

233 te infiltration and the clinical severity of EAE.

234 cifically resistant to the effector stage of EAE, and expression of interleukin (IL)-10 by PB plus PC

235 We collected fecal samples at key stages of EAE progression and quantified microbial abundances with

236 nd decline in numbers during later stages of EAE.

237 evelopment provides effective suppression of EAE and suggests the feasibility of a clinical approach

238 Furthermore, we examined UV suppression of EAE in mice devoid of the vitamin D receptor (VDR).

239 lts demonstrate that UV light suppression of EAE occurs in the absence of vitamin D production and in

240 examine whether the UV based suppression of EAE results, at least, in part from the production of vi

241 differentiation and ameliorates symptoms of EAE by decreasing Th17 cell-mediated inflammation and de

242 fect on attenuating the clinical symptoms of EAE.

243 particles had modest or negligible effect on EAE onset.

244 the importance of Fabp5/Canx interactions on EAE pathogenesis and on the patency of a model blood-bra

245 amin D, we studied the effect of UV light on EAE in mice unable to produce 7-dehydroxycholesterol (7-

246 Optimal EAE conditions extracted higher content of proanthocyani

247 hat miR-30d is enriched in the feces of peak EAE and untreated MS patients.

248 reover, NLPs ameliorated chronic progressive EAE in nonobese diabetic mice, a model which resembles s

249 ll-deficient mice, was sufficient to promote EAE recovery.

250 eg clonotypes that are equipped to recognize EAE-associated Ags.

251 APRIL before disease onset, shortly reduced EAE symptoms.

252 ination with NLRC3-overexpressed DCs reduces EAE progression.

253 B cells (B(regs)) has been shown to reverse EAE by promoting the expansion of peripheral and CNS-inf

254 ent, like Sb1 deletion, dramatically reverts EAE, strongly indicating that the CXCR6(+) T cells are t

255 naive mice and those exhibiting CP-EAE or RR-EAE revealed significantly diverse microbial populations

256 However, existing methods to score EAE disease severity are subjective and often vary betwe

257 lls, and IL-9R(-/-) mice develop more severe EAE compared with wild-type counterparts.

258 knockout for IL-9R, we show that more severe EAE in IL-9R(-/-) mice correlates with increased numbers

259 The more severe EAE in LysM (Cre) :Ppard (fl/fl) mice was associated wit

260 Here, we describe a variant of spontaneous EAE in the 2D2 T cell receptor transgenic mouse (2D2(+)

261 Relative to standard EAE scoring methods, IRAMS showed comparable measurement

262 disease severity and compared it to standard EAE scoring methods.

263 nhanced disease scoring compared to standard EAE scoring methods.

264 ermansia in turn increases Tregs to suppress EAE symptoms.

265 L-12Rbeta1, but not IL-12Rbeta2, to suppress EAE.

266 nderlying mechanism by which IL-9 suppresses EAE has not been clearly defined.

267 contrast, B-cell-deficiency attenuates TH17-EAE in the presence or absence of IFN-I treatment.

268 erimental autoimmune encephalomyelitis (TH17-EAE).

269 ce, IFN-I elevates IL-6 and exacerbates TH17-EAE.

270 We demonstrate that EAE, but not pregnancy, robustly increased TCR repertoir

271 t distribution by HPLC-SEC demonstrated that EAE extracted NEPs with high molecular weight.

272 lycolytic rates in T cells isolated from the EAE CNS correlate with upregulated expression of glycoly

273 ent of the glutamatergic transmission in the EAE cerebellum.

274 y, NLPs induced bystander suppression in the EAE model established in C57BL/6 x SJL F1 mice.

275 In the EAE model, the secondary amine 12 and the triazole 14 we

276 igodendrocyte death and myelin damage in the EAE model.

277 (PERK) activation on oligodendrocytes in the EAE model.

278 ockade led to a significant reduction in the EAE severity.

279 Adoptive transfer EAE studies linked this EAE phenotype in LysM (Cre) :Ppard (fl/fl) mice to heigh

280 Though EAE has been an effective screening tool for identifying

281 In addition to EAE, p40 also suppressed collagen-induced arthritis in m

282 ings define metabolic vulnerabilities due to EAE and provide evidence that behavioral changes and pri

283 D4 T cells after, but not before, CLP led to EAE disease equivalent to sham mice.

284 ficient mice commonly manifest resistance to EAE induction.

285 /6 mice deficient in GM-CSF are resistant to EAE induced by immunization with myelin oligodendrocyte

286 ient in GPR41 or GPR43 are more resistant to EAE pathogenesis.

287 ell priming, Sb1 (-/-) mice are resistant to EAE with a paucity of T helper (T(H)) cells that produce

288 e demonstrate that genetic susceptibility to EAE lies within the innate immune compartment.

289 :Ppard (fl/fl) mice were more susceptible to EAE and developed a more severe course of this disease c

290 Adoptive transfer EAE studies linked this EAE phenotype in LysM (Cre) :Ppa

291 CD4+ T cells from naive, EAE and CBD treated EAE mice by ChIP-seq.

292 ain at 37% lower levels than control-treated EAE mice, demonstrating that (18)F-FAC PET can monitor t

293 Fingolimod-treated EAE mice accumulate (18)F-FAC in the brain at 37% lower

294 Fingolimod-treated EAE mice were imaged with (18)F-FAC PET to assess if thi

295 nds appear to be enriched in mice undergoing EAE.

296 using CLEC12A knockout (KO) animals wherein EAE disease induction was delayed and reduced disease se

297 cells and IL-35 reduces pain associated with EAE by decreasing neuroinflammation and increasing myeli

298 nd IL-35 in attenuating pain associated with EAE independently of motor symptoms by decreasing neuroi

299 nd their metabolic functions associated with EAE susceptibility, implicating short-chain fatty acid m

300 Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes