ライフサイエンスコーパス: EAE

1 EAE mice were given subcutaneous injections of myelin ol

2 EAE scores were increased following ampicillin treatment

3 that the pathophysiology observed in active EAE was linked to the absence of ALCAM on BBB-ECs.

4 and provided equal clinical benefit in acute EAE in Nrf2(-/-) and WT mice, suggest that the antiinfla

5 ays in each cellular subset before and after EAE induction.

6 t Bhlhe40 expression was heterogeneous after EAE induction, with Bhlhe40-expressing cells displaying

7 ith a selective CRAC channel inhibitor after EAE onset ameliorated disease.

8 Bregs, BTLA(-/-) mice were protected against EAE.

9 tokine and Th2 responses, protection against EAE was independent of IL-4, IL-10, and Tregs.

10 ansion of eosinophils and protection against EAE was lost in IL-33(-/-) mice and upon neutralization

11 ced eosinophils conferred protection against EAE.

12 n FcgammaRs, as anti-CD48 did not ameliorate EAE or reduce the number of cytokine-producing effector

13 ectly target the myelin sheath to ameliorate EAE.

14 uced B220(+)CD5(+) Bregs greatly ameliorated EAE.

15 nse of WT Th17 cells and thereby ameliorated EAE.

16 nstrated that CD19 mAb treatment ameliorates EAE more effectively than does CD20 mAb.

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

18 , including T cell-mediated autoimmunity and EAE.

19 hibits more robust effects on Th17 cells and EAE.

20 rrespondent with reduced immune function and EAE CNS pathology.

21 paB activation on oligodendrocytes in MS and EAE remain unknown.

22 ependent synaptopathy typical of both MS and EAE.

23 paB activation on oligodendrocytes in MS and EAE.SIGNIFICANCE STATEMENT Multiple sclerosis (MS) is an

24 The combined SFE-CO2, PLE and EAE reduced antioxidant capacity of starting plant mater

25 both murine and human Th17 cells as well as EAE.

26 Accordingly, leukocyte infiltration at EAE onset is restricted to IL-1R1(+) subpial and subarac

27 ne receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antago

28 Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upr

29 volved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors.

30 -beta (IFNbeta)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate i

31 y, some of the sunblock preparations blocked EAE without UV radiation.

32 ssibly leading to excitotoxic damage in both EAE and MS diseases.

33 n astrocytes from spinal cord during chronic EAE involved decreases in expression of cholesterol synt

34 Clinical EAE is significantly attenuated in IL-1R-deficient and I

35 Nimodipine treatment attenuated clinical EAE and spinal cord degeneration and promoted remyelinat

36 of plasminogen and fibrinogen had decreased EAE severity, they did not exhibit the delay in EAE dise

37 d Th17 differentiation, leading to decreased EAE.

38 lysis and CNS inflammation in four different EAE models, including the 2D2 TCR-transgenic mouse model

39 During EAE, both wild type and CCR7-/- CD11c-eYFP cells infiltr

40 role and cellular source of IL-1beta during EAE pathogenesis are poorly defined.

41 rve as critical producers of IL-1beta during EAE, with this cytokine inducing response in both hemato

42 r sources of IL-1beta and its actions during EAE, in both lymphoid tissues and within the CNS.

43 thological hallmark of MS lesions and during EAE, with myelin antigen processing and T cell pathogeni

44 cholesterol synthesized by astrocytes during EAE and MS is discussed.

45 feature of pathogenic CD4(+) T cells during EAE and point to CD48 as a potential target for immunoth

46 ing pathogenic CD48(++)CD4(+) T cells during EAE.

47 ls highly upregulated CD48 expression during EAE and were enriched for pathogenic CD4(+) T cells.

48 Administration of CCL1-Ig during EAE enhanced the in vivo proliferation of these CCR8(+)

49 ogliosis in response to neural injury during EAE.

50 Administration of anti-CD48 mAb during EAE attenuated clinical disease, limited accumulation of

51 catenin activity in CNS blood vessels during EAE progression correlates with up-regulation of neurona

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

53 Whereas mice with either EAE alone or influenza alone survived, 70% of comorbid m

54 In experimental autoimmune encephalitis (EAE), autoimmune T cells are activated in the periphery

55 diated experimental autoimmune encephalitis (EAE).

56 n experimental autoimmune encephalomyelitis (EAE) and in in vitro studies regarding the effect of the

57 f experimental autoimmune encephalomyelitis (EAE) and induction of tolerance.

58 n experimental autoimmune encephalomyelitis (EAE) and perhaps MS.

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

60 f experimental autoimmune encephalomyelitis (EAE) as a result of an increase of protective regulatory

61 d experimental autoimmune encephalomyelitis (EAE) can be achieved with myelin oligodendrocyte glycopr

62 n experimental autoimmune encephalomyelitis (EAE) disease model, we found that OX40 stimulation inhib

63 d experimental autoimmune encephalomyelitis (EAE) disease scores via the ligand-activated transcripti

64 s experimental autoimmune encephalomyelitis (EAE) disease severity.

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

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

67 e experimental autoimmune encephalomyelitis (EAE) in animals.

68 g experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice, a well-studied model of MS, we sho

69 e experimental autoimmune encephalomyelitis (EAE) in mice.

70 g experimental autoimmune encephalomyelitis (EAE) induction, Treg-specific Il27ra(-/-) mice develop m

71 d experimental autoimmune encephalomyelitis (EAE) is unclear.

72 g experimental autoimmune encephalomyelitis (EAE) mice.

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

74 e experimental autoimmune encephalomyelitis (EAE) model, we were able to study not only evoked hypera

75 e experimental autoimmune encephalomyelitis (EAE) model.

76 e experimental autoimmune encephalomyelitis (EAE) models in the common marmoset and rhesus monkey to

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

78 e experimental autoimmune encephalomyelitis (EAE) mouse model.

79 s experimental autoimmune encephalomyelitis (EAE) severity and relapse incidence.

80 d experimental autoimmune encephalomyelitis (EAE) using AhR knockout mice.

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

82 h experimental autoimmune encephalomyelitis (EAE) were administered a sublethal dose of influenza.

83 f experimental autoimmune encephalomyelitis (EAE) with hippocampal degeneration in C57BL/6 mice, in w

84 m experimental autoimmune encephalomyelitis (EAE), a model of MS.

85 n experimental autoimmune encephalomyelitis (EAE), a mouse model of MS.

86 e experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis.

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

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

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

90 f experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), throug

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

92 d experimental autoimmune encephalomyelitis (EAE), but how it impacts neuroinflammation is poorly und

93 f experimental autoimmune encephalomyelitis (EAE), deletion of Rac1 in T cells exhibits more robust e

94 , experimental autoimmune encephalomyelitis (EAE), expansion of pathogenic, myelin-specific Th1 cell

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

96 e experimental autoimmune encephalomyelitis (EAE), miRNA dysregulation has been mainly related to imm

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

98 d experimental autoimmune encephalomyelitis (EAE), the C-C chemokine receptor 6 (CCR6) is critical fo

99 , experimental autoimmune encephalomyelitis (EAE), the mechanisms of how these cells recognize their

100 n experimental autoimmune encephalomyelitis (EAE), the most studied animal model of multiple sclerosi

101 s experimental autoimmune encephalomyelitis (EAE), the mouse model of MS.

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

103 l experimental autoimmune encephalomyelitis (EAE).

104 o experimental autoimmune encephalomyelitis (EAE).

105 f experimental autoimmune encephalomyelitis (EAE).

106 g experimental autoimmune encephalomyelitis (EAE).

107 , experimental autoimmune encephalomyelitis (EAE).

108 f experimental autoimmune encephalomyelitis (EAE).

109 l experimental autoimmune encephalomyelitis (EAE).

110 , experimental autoimmune encephalomyelitis (EAE).

111 g experimental autoimmune encephalomyelitis (EAE).

112 f experimental autoimmune encephalomyelitis (EAE).

113 , experimental autoimmune encephalomyelitis (EAE).

114 l experimental autoimmune encephalomyelitis (EAE).

115 l experimental autoimmune encephalomyelitis (EAE).

116 n experimental autoimmune encephalomyelitis (EAE).

117 , experimental autoimmune encephalomyelitis (EAE).

118 g experimental autoimmune encephalomyelitis (EAE).

119 f experimental autoimmune encephalomyelitis (EAE).

120 n experimental autoimmune encephalomyelitis (EAE).

121 d experimental autoimmune encephalomyelitis (EAE).

122 , experimental autoimmune encephalomyelitis (EAE).

123 d experimental autoimmune encephalomyelitis (EAE).

124 e Experimental Autoimmune Encephalomyelitis (EAE).

125 l experimental autoimmune encephalomyelitis (EAE).

126 , experimental autoimmune encephalomyelitis (EAE).

127 o experimental autoimmune encephalomyelitis (EAE).

128 n experimental autoimmune encephalomyelitis (EAE, an animal model for multiple sclerosis [MS]).

129 [experimental autoimmune encephalomyelitis, (EAE)] and a stabilized version of mouse CCL1 (CCL1-Ig).

130 (experimental autoimmune encephalomyelitis; EAE), but the mechanisms remain obscure.

131 When we treated mice exhibiting established EAE with 6-ECDCA, or the natural FXR ligand chenodeoxych

132 hey remain in the CNS in situ and exacerbate EAE.

133 ient CD11c-eYFP cells in the CNS exacerbated EAE.

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

135 iquids, PLE, and enzyme-assisted extraction, EAE, have been tested to improve the extraction of phlor

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

137 We found that following EAE induction, pertussis toxin administration leads to I

138 lycoprotein (MOG) peptide 35-55 (p35-55) for EAE induction and treated with oral DMF or vehicle daily

139 en 1.74 +/- 0.11 and 2.93 +/- 0.15 %ID/g for EAE mice, compared with 1.25 +/- 0.08 and 2.24 +/- 0.11

140 Spinal cords from EAE-challenged Plg(-) mice demonstrated significantly de

141 Optic nerve from EAE and optic chiasm from MS also showed decreased chole

142 e in both the pathogenesis and recovery from EAE.

143 activating Tregs to facilitate recovery from EAE.

144 16 (peak clinical severity) CNS samples from EAE mice had prominent representation of inflammatory pe

145 erred, MOG-specific T cells was able to halt EAE progression after disease onset.

146 from development of clinical and histologic EAE.

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

148 The impaired EAE disease can be explained by the reduced proliferatio

149 In EAE-afflicted mice, minocycline treatment significantly

150 s, indicating an important role for MKP-2 in EAE development.

151 old increase of nanoparticle accumulation in EAE compared with healthy controls, P < 0.001).

152 defines a PTX-IL-1-Bhlhe40 pathway active in EAE.

153 in the CSF of patients with active MS and in EAE brains.

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

155 tion of EMMPRIN on T cells in culture and in EAE mice, correspondent with reduced immune function and

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

157 severity, they did not exhibit the delay in EAE disease onset, as seen in mice with plasminogen defi

158 core, CNS inflammation, and demyelination in EAE was abolished in AhR(-/-) mice.

159 ives chronic tissue damage and disability in EAE via pleiotropic pathways, but it is dispensable duri

160 ype hypersensitivity and clinical disease in EAE mouse models.

161 chanism that leads to miRNA dysregulation in EAE/MS.

162 spinal CaMKIIalpha activity was enhanced in EAE, correlating with the development of ongoing spontan

163 with the latter dominant over the former in EAE, highlighting this adaptor as a potential novel targ

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

165 anical allodynia and thermal hyperalgesia in EAE.

166 d mechanical and thermal hypersensitivity in EAE mice.

167 inal cord is sufficient to induce illness in EAE-resistant IL-1beta knockout (KO) mice.

168 necessary for the efficacy of laquinimod in EAE and that laquinimod may represent a first-in-class d

169 tially abrogates the effect of laquinimod in EAE.

170 d iNOS and reactive oxygen species levels in EAE.

171 Inhibition of miR-142-3p, locally in EAE brain and in a MS chimeric ex vivo model, recovered

172 that IL-17 contributes to persistent pain in EAE and functions as an upstream regulator of CaMKIIalph

173 as critical regulators of persistent pain in EAE, which may ultimately offer new therapeutic targets

174 taneous pain and evoked hyperalgesia pain in EAE.

175 esis is necessary for disease progression in EAE and that treatment with 4-MU may be a potential ther

176 further investigation of (64)Cu-rituximab in EAE models and consideration of use in MS patients to ev

177 fic T cells that are known to play a role in EAE pathogenesis.

178 s showing protective and pathogenic roles in EAE.

179 that is mediated by CaMKIIalpha signaling in EAE.

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

181 ls in MS changed their expression in vivo in EAE upon supplementation, supporting the hypothesis that

182 reated DCs, which failed to passively induce EAE.

183 To induce EAE, C57/BL6 mice were immunized with the Hooke lab MOG

184 gnificant amelioration of PLP178-191-induced EAE.

185 a classical co-adjuvant for actively induced EAE, promoted IL-1beta production by myeloid cells in th

186 sted in the myelin oligoglycoprotein-induced EAE mouse model of multiple sclerosis.

187 In the inflamed EAE spinal cord however, the patterns of expressions wer

188 ted NAg-specific sensitization and inhibited EAE in C57BL/6 mice in pretreatment and therapeutic regi

189 vitro IFN-beta + MOG-induced Tregs inhibited EAE when transferred into actively challenged recipients

190 + OVA in Alum-specific vaccination inhibited EAE elicited by OVA + MOG in CFA but not EAE elicited by

191 ransfer of PD-L1(+)/PD-L2(+) AAMvarphis into EAE induced mice reduced disease incidence, delayed dise

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

193 ich AMPK modulates inflammatory disease like EAE.

194 s IL-1beta production during T(H)17-mediated EAE pathogenesis.

195 4(+) T cells was necessary for DHEA-mediated EAE amelioration, as well as for direct downregulation o

196 rimental autoimmune encephalomyelitis model (EAE).

197 n, we disclose the efficacy of 4a in a mouse EAE model, which is comparable to 4c (FTY720).

198 Confocal in vivo imaging of the mouse EAE spinal cord reveals that impaired neurological funct

199 inflammation and synaptic alterations in MS/EAE are still unknown.

200 uting to excitotoxic neurodegeneration in MS/EAE.

201 Although neurons in the non EAE spinal cords did not show the IGF-I immunoreactivity

202 ted EAE elicited by OVA + MOG in CFA but not EAE elicited by MOG in CFA.

203 n turn, leading to the rapid amelioration of EAE.

204 duced both TLR2 tolerance and attenuation of EAE.

205 B cells can be detected in the CNS of EAE mice using (64)Cu-rituximab PET.

206 activity of triterpenoids in the context of EAE.

207 The clinical course of EAE is not improved by the solTNF inhibitor XPro1595 in

208 e with EAE but did not affect development of EAE or local microglial activation.

209 ) CD4cre(tg) mice developed a milder form of EAE.

210 PET imaging of EAE and control mice was performed 1, 4, and 19 h after

211 cific T cells did not alter the incidence of EAE or the trajectory of its initial clinical course, bu

212 eatment with 4-MU decreases the incidence of EAE, delays its onset, and reduces the severity of estab

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

214 ical analyses revealed that the induction of EAE led to a surprising alteration of the lung milieu, c

215 n to be crucial factors for the induction of EAE.

216 fere with the CNS-restricted inflammation of EAE by reprogramming infiltrating MCs into antiinflammat

217 Initiation of EAE or subdural injection of IL-1beta induces a similar

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

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

220 Finally, in transfer models of EAE, 3-BrPa robustly attenuates the encephalitogenic pot

221 -191 attenuate CNS autoimmunity in models of EAE, implicating the potential of this approach as a nov

222 oteolipid protein- and MOG-induced models of EAE, respectively, and was abrogated by pretreatment wit

223 , but not in microglia, delayed the onset of EAE in challenged animals and was associated with reduce

224 ls in the spinal cord and lymphoid organs of EAE mice were increased compared with naive controls, in

225 ry of TGF-beta2 during the effector phase of EAE ameliorated disease severity.

226 attenuates the encephalitogenic potential of EAE-driving immune cells.

227 set exacerbates the clinical presentation of EAE, CD4(+) T-cell infiltration into the CNS, and demyel

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

229 2 is essential to the pathogenic response of EAE, and it acts mainly via regulating the important ant

230 significantly reduced the clinical scores of EAE and attenuated mechanical allodynia and thermal hype

231 S60 has been shown to reduce the severity of EAE by dampening the immune response and myelin loss.

232 so witnessed in the lessening of severity of EAE clinical scoring, indicating an in vivo functional r

233 1KO macrophages showed decreased severity of EAE compared with mice receiving wild-type or CSL/RBP-Jk

234 e onset and reduces the clinical severity of EAE induced by myelin-specific CD4(+) T cells.

235 of anti-EMMPRIN Abs reduces the severity of EAE.

236 ry properties that decreases the severity of EAE; it was recently found to attenuate the conversion f

237 significant delay and diminished symptoms of EAE by oral administration.

238 which likely reduce the clinical symptoms of EAE.

239 ntribute to EAE's pathogenesis, treatment of EAE mice with MOG-psigma1, but not OVA-psigma1, resulted

240 lutamatergic synaptic enhancement typical of EAE/MS.

241 ver, our documentation of an M-SOB effect on EAE susceptibility in mice allows for modeling and detai

242 We also show that the M-SOB effect on EAE susceptibility is associated with differential produ

243 ng in the efficacious suppression of ongoing EAE.

244 ization with this epitope suppressed ongoing EAE, which was abrogated by CD8(+) T cell depletion.

245 Passive EAE transfer experiments suggested that the pathophysiol

246 BTLA(-/-) mice showed more pronounced EAE with fewer Tregs, but upon adoptive transfer of MOG-

247 OX40 stimulation inhibited IL-17 and reduced EAE.

248 Indeed, MKP-2(-/-) mice developed reduced EAE severity, associated with diminished CNS immune cell

249 t mutation mice showed significantly reduced EAE clinical scores, an absence of evoked pain, and ongo

250 i-CD20 therapy likely contribute to residual EAE severity by producing autoreactive Abs.

251 dent and interferon-beta (IFNbeta)-resistant EAE (termed type B EAE), whereas EAE induced by weak act

252 tory mechanism by which an IFNbeta-resistant EAE subtype develops.

253 These induced Bregs restored EAE Treg function in a BTLA-dependent manner.

254 6a-deficient 2D2 T cells induced more severe EAE and were more prone to differentiate into Th17 cells

255 pecific Il27ra(-/-) mice develop more severe EAE.

256 reparations had variable ability to suppress EAE.

257 s the components responsible for suppressing EAE.

258 vivo functional role for TSPO in suppressing EAE.

259 n T and B cells at pre- and post-symptomatic EAE stages.

260 cing and bioinformatics analyses showed that EAE-induced gene expression changes differed between neu

261 unization with such epitopes ameliorates the EAE.

262 These T cells drive the EAE pathogenesis to irreversible neurologic deficit.

263 olve in pathophysiological events during the EAE.

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

265 production in immune cells isolated from the EAE CNS.

266 These findings from the EAE model should inspire efforts toward investigating th

267 ent of the glutamatergic transmission in the EAE cerebellum.

268 te glycoprotein (MOG), an autoantigen in the EAE model.

269 the total GSK3beta expressing neurons in the EAE spinal cord, it is conceivable that the intense tota

270 he CD4(+) and CD8(+) T cells that invade the EAE CNS are highly glycolytic.

271 s study, we examined the spinal cords of the EAE, the animal model of multiple sclerosis, to see if t

272 Although inflammatory B cells contribute to EAE's pathogenesis, treatment of EAE mice with MOG-psigm

273 ytes increased the susceptibility of mice to EAE (female mice).

274 ce expressing RORgammat(M) were resistant to EAE associated with defective TH17 differentiation but m

275 nondiseased CNS, are completely resistant to EAE development following adoptive transfer of myelin-sp

276 /6 mice deficient in GM-CSF are resistant to EAE induced by immunization with myelin oligodendrocyte

277 We show that susceptibility to EAE requires activation of IL-1R1 on radiation-resistant

278 eceptor, the mice regained susceptibility to EAE, demonstrating that IFN-gamma signaling in DCs media

279 e lowest birth rate were less susceptible to EAE than mice born during the M-SOB with the highest bir

280 e deletion rendered mice more susceptible to EAE.

281 controversial in models of adoptive transfer EAE in which no adjuvant and no TLR ligands are administ

282 low-level TLR2 ligands in adoptive transfer EAE induces TLR2 tolerance and attenuates disease.

283 In adoptive transfer EAE models, Bhlhe40-deficient Th1 and Th17 cells were bo

284 od for TLR2 involvement in adoptive transfer EAE.

285 inery, and impairs their ability to transfer EAE.

286 imed by the epitope immunization transferred EAE suppression.

287 spleen transcripts from minocycline-treated EAE mice had a significantly lower MMP-9/TIMP-1 ratio, a

288 sigma1-treated EAE or Bregs from PBS-treated EAE mice did not resolve disease, whereas the adoptive t

289 20(+)CD5(-) B cells from MOG-psigma1-treated EAE or Bregs from PBS-treated EAE mice did not resolve d

290 significantly higher compared with wild-type EAE and were characterized as IL-17 (IL-17 and GM-CSF do

291 We found that, unexpectedly, EAE was less severe in Rai(-/-) mice compared with their

292 analysis in Tob1(-/-) and wildtype mice upon EAE.

293 )-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requir

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

295 f flavonoid-containing polar extracts, while EAE added 20.2% (w/w) of water-soluble constituents and

296 cells in culture and in mice afflicted with EAE.

297 the brains and spinal cords of alpha1KO with EAE were significantly higher compared with wild-type EA

298 e onset of neuroinflammation associated with EAE.

299 tive synapse loss in hippocampi of mice with EAE but did not affect development of EAE or local micro

300 AMPKalpha1 knockout (alpha1KO) mice with EAE showed severe demyelination and inflammation in the