ライフサイエンスコーパス: MOG

1 0-48 of myelin oligodendrocyte glycoprotein (MOG).

2 antigen myelin oligodendrocyte glycoprotein (MOG).

3 en L.FFG and right middle occipital gyrus (R.MOG).

4 erleaved with practice (micro-offline gains, MOGs).

5 +) T cells express a functional receptor for MOG.

6 ted mixed chimeras together with BM-encoding MOG.

7 ated at loops connecting the beta strands of MOG.

8 ysin (2.0%), ARHGAP26 (1.3%), CASPR2 (0.9%), MOG (0.8%), GAD65 (0.5%), Ma2 (0.5%), Yo (0.4%), and Ma1

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

10 godendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administered into either T

11 myelin oligodendrocyte glycoprotein epitope MOG(35-55) or the full-length recombinant human MOG prot

12 i-CD3 enhanced oral tolerance induced by fed MOG(35-55) peptide, resulting in less severe experimenta

13 myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) revealed an ameliorated disease course in co

14 Unlike MOG(35-55), where lack of B cells yields more severe dis

15 ous relapsing-remitting disease phenotype in MOG(35-55)-immunized C57BL/6 mice.

16 ression was associated with the expansion of MOG(35-55)-specific FoxP3(+) regulatory T cells (Treg ce

17 ith a profound reduction of proliferation of MOG(35-55)-specific Th1 and Th17 cells.

18 are specific for the inducing myelin peptide MOG(35-55).

19 myelin oligodendrocyte glycoprotein epitope (MOG)35-55 as well as an epitope within the axonal protei

20 -191 or myelin oligodendrocyte glycoprotein (MOG)35-55 in proteolipid protein- and MOG-induced models

21 rity in myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-induced EAE, and reduced inflammation

22 on with myelin oligodendrocyte glycoprotein (MOG)35-55 The mechanism of action of GM-CSF in EAE is po

23 ells in myelin oligodendrocyte glycoprotein (MOG)35-55-induced EAE.

24 severe myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyeli

25 ce with myelin oligodendrocyte glycoprotein (MOG)(35-55) Ig-like transcript 3 (ILT3) is an inhibitory

26 pe from myelin oligodendrocyte glycoprotein (MOG)(35-55) induced tolerogenic dendritic cells and supp

27 murine myelin oligodendrocyte glycoprotein (MOG)-(35-55)-specific line T-cells to the same extent as

28 , resulting in a novel therapeutic, DRalpha1-MOG-35-55, that within the limitations of the EAE model

29 ecific (myelin oligodendrocyte glycoprotein [MOG]35-55) T cell response.

30 ension (myelin oligodendrocyte glycoprotein [MOG]-35-55 peptide) that provided secondary structure no

31 Myelin oligodendrocyte glycoprotein (MOG), a constituent of central nervous system myelin, is

32 Here, we present MetaOmGraph (MOG), a free, open-source, standalone software for explo

33 ated peripheral blood mononuclear cells from MOG-AAD patients by flow cytometry and found a strong an

34 FAIP3 levels are associated with relapses in MOG-AAD patients, which may have clinical utility as a d

35 ls at relapse compared to remission state in MOG-AAD patients.

36 ulated at a relapse compared to remission in MOG-AAD patients.

37 MOG-antibody associated disease (MOG-AAD) is a recently recognized demyelinating disorder

38 alue in myelin oligodendrocyte glycoprotein (MOG)-ab positive and ab-negative NMOSD.

39 Myelin oligodendrocyte glycoprotein (MOG)-Ab was detected in seven; two with acute disseminat

40 tive, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unk

41 the current knowledge of MOG, the metrics of MOG-Ab assays and the clinical associations identified.

42 = 40.9-86.5) of nonrelapsing children became MOG-Ab negative compared to 14.1% (95% CI = 4.7-38.3) of

43 lly, children with monophasic disease become MOG-Ab negative earlier than relapsing children, but thi

44 f 87.1% against AQP4-ab NMOSD, 95.2% against MOG-ab NMOSD and 87.5% in the heterogenous ab-negative N

45 b) dynamics between children and adults with MOG-Ab-associated disease (MOGAD).

46 MOG-Ab-associated disease is different to AQP4-Ab-positi

47 We also highlight differences between MOG-Ab-associated disease, NMOSD and MS, and describe ou

48 r current understanding on how best to treat MOG-Ab-associated disease.

49 MOG-Ab-positive patients more frequently presented with

50 nt of AQP4-Ab-positive patients but only 44% MOG-Ab-positive patients were females (P = .02) with a t

51 Twenty AQP4-Ab-positive patients and 9 MOG-Ab-positive patients were identified.

52 bstrate enabled identification of a group of MOG-Ab-positive patients with demyelinating phenotypes.

53 patients with NMOSD (31 AQP4-ab-positive, 21 MOG-ab-positive, 16 ab-negative) or MS (44) were selecte

54 tive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), opti

55 The majority of human anti-MOG Abs did not recognize rodent MOG, which has implicat

56 assays has re-invigorated the examination of MOG-Abs and their role in autoimmune and demyelinating d

57 ponses to treatment that are associated with MOG-Abs are currently being defined.

58 Despite the fact that patients with MOG-Abs can fulfill the diagnostic criteria for NMO, the

59 we showed that patients with NMO/NMOSD with MOG-Abs demonstrate differences when compared with patie

60 ffer between the 2 groups, but patients with MOG-Abs had better outcomes from the onset episode, with

61 Additionally, patients with MOG-Abs had more favorable outcomes.

62 Further studies identified MOG-Abs in adults and children with ADEM, seizures, ence

63 ford NMO service and who tested positive for MOG-Abs or AQP4-Abs were included in the study.

64 Initially, MOG-Abs were reported in children with acute disseminate

65 lin-oligodendrocyte glycoprotein antibodies (MOG-Abs) have been found in some patients.

66 igodendrocyte glycoprotein (MOG) antibodies (MOG-Abs) were first detected by immunoblot and enzyme-li

67 test patient serum samples for AQP4-Abs and MOG-Abs.

68 4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

69 of lymphocytes was reduced and apoptosis of MOG-activated CD4+ T cells was increased in kirenol trea

70 ary CD4(+) T cell response to the inoculated MOG Ag.

71 IgG and myelin-oligodendrocyte glycoprotein (MOG)-alpha1-IgG.

72 GMCSF-MOG also retained dominant inhibitory activity when dire

73 Furthermore, immune tolerization against MOG ameliorated symptoms.

74 fic for myelin oligodendrocyte glycoprotein (MOG), an autoantigen in the EAE model.

75 growth factor (NGF) as a binding partner for MOG and demonstrate that this interaction is capable of

76 ased assays using C-terminal-truncated human MOG and full-length M23-AQP4 were used to test patient s

77 s into recipient mice after the cocapture of MOG and hemagglutinin leads to the production of class-s

78 genes, myelin oligodendrocyte glycoprotein (Mog) and ermin (Ermn), and by immunohistochemistry for m

79 ng between posterior visual regions (L.FFG-R.MOG) and greater functional segregation between task-pos

80 termined the presence of antibodies to AQP4, MOG, and GlyR using cell-based assays.

81 MOG antibodies (median 1:2560; range 1:160-1:20 480) wer

82 fferent compared to that of children without MOG antibodies (p=0.003; and p=0.032, respectively).

83 ad a worse visual outcome than patients with MOG antibodies alone (median visual score, 0 [range, 0-5

84 d in 2 of 10 (20%) relapses in patients with MOG antibodies and 12 of 13 (92.5%) with AQP4 antibodies

85 In 16 patients with MOG antibodies and 29 with AQP4 antibodies, mean follow-

86 Children with MOG antibodies did not differ in their age at presentati

87 orest visual outcomes, whereas patients with MOG antibodies had a better outcome that was similar to

88 All 19 children with MOG antibodies had a uniform MRI pattern, characterised

89 In addition, children with MOG antibodies had involvement of more anatomical areas

90 atients with GlyR antibodies concurrent with MOG antibodies had recurrent isolated ON, and the patien

91 detected only in the 50 anti-NMDAR patients, MOG antibodies in 3 of 50 anti-NMDAR and 1 of 56 NMO pat

92 Patients with ADEM with MOG antibodies in our cohort had a uniform MRI character

93 onnecting the infection to the production of MOG antibodies remains a mystery.

94 autoimmune encephalitis in cohort B (n=64), MOG antibodies were more common than all neuronal antibo

95 psing demyelinating episodes associated with MOG antibodies were observed only in children with MOG a

96 ca, 37 (77%) had AQP4 antibodies, 4 (8%) had MOG antibodies, 2 (4%) had AQP4 antibodies concurrent wi

97 es occurred in 6 of 16 (37.5%) patients with MOG antibodies, and 13 occurred in 7 of 29 (24%) with AQ

98 , 2 (4%) had AQP4 antibodies concurrent with MOG antibodies, and 5 (10%) were seronegative.

99 ads to the production of class-switched anti-MOG antibodies, dependent on the presence of hemagglutin

100 116 patients had MOG antibodies, including 94 (39%) from cohort A and 22

101 emyelinating and encephalitic syndromes with MOG antibodies, their response to treatment, and the phe

102 magglutinin-specific T cells to produce anti-MOG antibodies.

103 tiary centres in Spain were investigated for MOG antibodies.

104 ical outcome in contrast to children lacking MOG antibodies.

105 nt (p=0.038), compared with children without MOG antibodies.

106 tibodies were observed only in children with MOG antibodies.

107 Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies (MOG-Abs) were first detected by immunob

108 ions of myelin oligodendrocyte glycoprotein (MOG) antibodies are usually focused on demyelinating syn

109 Myelin oligodendrocyte glycoprotein (MOG) antibodies have been recently described in children

110 tion cohort, 65 adults and 18 children) with MOG antibody (n = 26), AQP4 antibody disease (n = 26) an

111 Multiple sclerosis was discriminated from MOG antibody disease and from AQP4 antibody disease with

112 Best classifiers between MOG antibody disease and multiple sclerosis were similar

113 Brain imaging characteristics of MOG antibody disease are largely unknown and it is uncle

114 r distinction between multiple sclerosis and MOG antibody disease both considered primary demyelinati

115 y disease with high predictive values, while MOG antibody disease could not be accurately discriminat

116 Adults and children with MOG antibody disease frequently had fluffy brainstem les

117 MOG antibody disease spontaneously separated from multip

118 The overlap between MOG antibody oligodendrocytopathy and AQP4 antibody astr

119 ), fluffy lesions and three lesions or less (MOG antibody).

120 In MOG antibody-associated disorder, the efficacy of RTX is

121 be used to improve treatment strategies for MOG antibody-associated disorder.

122 nating syndromes, but the entire spectrum of MOG antibody-associated syndromes in children is unknown

123 The spectrum of paediatric MOG antibody-associated syndromes is wider than previous

124 All MOG antibody-positive cases were included in our study,

125 se, and myelin oligodendrocyte glycoprotein (MOG) antibody (Ab) dynamics between children and adults

126 MOG-antibody associated disease (MOG-AAD) is a recently

127 , or recurrent isolated ON had antibodies to MOG, AQP4, or GlyR.

128 Hemagglutinin and MOG are both presented to T cells, which in turn are act

129 against myelin oligodendrocyte glycoprotein (MOG) are associated with autoimmune central nervous syst

130 intact myelin oligodendrocyte glycoprotein (MOG) are found in different inflammatory diseases of the

131 Use of cell-based assays with native MOG as the substrate enabled identification of a group o

132 15-35 is immunogenic and cross-reactive with MOG at the polyclonal level, it fails to expand a thresh

133 quiet rest periods and predicts the level of MOGs before asymptotic performance is achieved.

134 ining of DCs in vitro with purified scFv DEC:MOG, binding to DCs and colocalization with MHC class II

135 n, 7 adults) who recognized cell-bound human MOG, but had different diseases, including acute dissemi

136 bs are not focused on one specific region of MOG, but instead target multiple epitopes.

137 We illustrate MOG by case studies of large curated datasets from human

138 f the target cell, it can be cocaptured with MOG by MOG-specific B cells via the B-cell receptor.

139 when Ig-myelin oligodendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administ

140 ying two siblings, aged 6 and 11 years, with MOGS-CDG and biallelic MOGS (mannosyl-oligosaccharide gl

141 was much longer than the previous report of MOGS-CDG, in a child who died at 74 days of age.

142 cosylation type IIb (CDG-IIb), also known as MOGS-CDG.

143 Internalized MOG colocalized with autophagosomes, which can protect f

144 ase pathogenesis, because it could result in MOG cross linking on oligodendrocytes and/or immune comp

145 tasis in the healthy human brain through the MOG-DC-SIGN homeostatic regulatory axis, which is compri

146 ramarginal gyrus and middle occipital gyrus (MOG) during action execution, and in pars opercularis IF

147 The most frequently recognized MOG epitope was revealed by the P42S mutation positioned

148 ominant myelin oligodendrocyte glycoprotein (MOG) epitope (residues 40-48) against destructive proces

149 The targeting of different MOG epitopes by encephalitogenic Abs has implications fo

150 OG-specific B cells take up large amounts of MOG from cell membranes.

151 ed with myelin oligodendrocyte glycoprotein (MOG) fused to reovirus protein sigma1 (MOG-psigma1), whi

152 An anti-beta-galactosidase scFv:MOG fusion protein (scFv GL117:MOG) served as isotype co

153 Upon mutation analysis, we detected multiple MOGS genotypes including wild-type alleles in their cult

154 To date, the exact function of MOG has remained unknown, with MOG knockout mice display

155 clonal Tregs for any self-antigen, let alone MOG, has not been analyzed in the periphery or at the si

156 fic for myelin oligodendrocyte glycoprotein (MOG) have been detected in patients with multiple sclero

157 in Rras2(-/-) mice have reduced affinity for MOG/I-A(b) tetramers, suggesting that enhanced negative

158 Patients who rapidly lost their anti-MOG IgG still generated a long-lasting IgG response to v

159 At a population level, AQP4-IgG and MOG-IgG account for 9% of optic neuritis and are associa

160 er were analysed using cell-based assays for MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG).

161 Sera were tested for AQP4-IgG and MOG-IgG by using a live-cell-based flow cytometry assay.

162 Patients with MOG-IgG had neuromyelitis optica spectrum disorder (NMOS

163 year follow-up suggested that persistence of MOG-IgG is associated with relapses.

164 d are associated with recurrent attacks, but MOG-IgG optic neuritis has a better visual outcome than

165 sions in a prospective incident cohort of 74 MOG-IgG positive children with serial MRI scans over a m

166 Silent new lesions were detected in 14% of MOG-IgG positive participants, most commonly within the

167 apses were seen in patients when they became MOG-IgG seronegative, whereas a persistent positive sero

168 ith: (1) characteristic MOGAD phenotype, (2) MOG-IgG seropositivity by live cell-based assay and (3)

169 MOG-IgG serostatus was longitudinally assessed in seropo

170 e also investigate the clinical relevance of MOG-IgG through a longitudinal analysis of serological s

171 jority of children showed a decline of serum MOG-IgG titres over time.

172 godendrocyte glycoprotein immunoglobulin G1 (MOG-IgG) and associated clinical features of patients fr

173 igodendrocyte glycoprotein immunoglobulin G (MOG-IgG) antibodies are associated clinically with eithe

174 against myelin-oligodendrocyte glycoprotein (MOG-IgG) have been increasingly recognised as a new type

175 Among patients with MOG-IgG, Japanese tended to have a monophasic milder dis

176 diagnosis was MS in 57%, idiopathic in 29%, MOG-IgG-associated disorder in 5%, AQP4-IgG-seropositive

177 d ethnic differences in clinical profiles of MOG-IgG-associated disorders between East Asian (Japanes

178 aphic, clinical and therapeutic data from 68 MOG-IgG-positive adults were collected (Japanese, n=44;

179 Among MOG-IgG-positive patients, 4 of 6 patients had recurrent

180 was most commonly observed in patients with MOG-IgG.

181 CNS inflammatory diseases were positive for MOG-IgG.

182 use of atypical optic neuritis: AQP4-IgG and MOG-IgG.

183 MOG-IgG1 was identified in 25% of RION, 25% of CRION, 10

184 ng from myelin oligodendrocyte glycoprotein (MOG) immunization.

185 e identified in 23 patients (45%), including MOG in 10 patients, AQP4 in 6 patients, and GlyR in 7 pa

186 nts, and GlyR in 7 patients (concurrent with MOG in 3 and concurrent with AQP4 in 1).

187 vaccination inhibited EAE elicited by OVA + MOG in CFA but not EAE elicited by MOG in CFA.

188 by OVA + MOG in CFA but not EAE elicited by MOG in CFA.

189 d Tregs displayed overlapping affinities for MOG in the periphery, yet in the CNS, the site of neuroi

190 during myelin oligodendrocyte glycoprotein (MOG)-induced EAE would improve the clinical course of di

191 tion in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (

192 ce from myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (

193 odel of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (

194 osages of CCL2 were effective in suppressing MOG-induced experimental autoimmune encephalomyelitis (E

195 bunits of NOX2 were partially protected from MOG-induced experimental autoimmune encephalomyelitis an

196 erance against the subsequent development of MOG-induced experimental autoimmune encephalomyelitis in

197 eletion specifically in DCs are resistant to MOG-induced experimental autoimmune encephalomyelitis.

198 otein (MOG)35-55 in proteolipid protein- and MOG-induced models of EAE, respectively, and was abrogat

199 In vitro IFN-beta + MOG-induced Tregs inhibited EAE when transferred into ac

200 Notably, GMCSF-MOG inhibited EAE when coinjected adjacent to the MOG35-

201 We next injected scFv DEC:MOG into mice and observed elevated numbers of highly ac

202 Here, we show that, in healthy human myelin, MOG is decorated with fucosylated N-glycans that support

203 ding region of the immunodominant peptide of MOG is susceptible to cleavage by the NOX2-controlled cy

204 MOGS is expressed in the endoplasmic reticulum and is in

205 Myelin oligodendrocyte glycoprotein (MOG) is a central nervous system myelin-specific molecul

206 7/BL6 mice were immunized with the Hooke lab MOG kit, sacrificed at the peak of the disease and their

207 t function of MOG has remained unknown, with MOG knockout mice displaying normal myelin ultrastructur

208 6 and 11 years, with MOGS-CDG and biallelic MOGS (mannosyl-oligosaccharide glucosidase) mutations (G

209 Binding of NGF to MOG may offer widespread implications into mechanisms th

210 iations with five genes (ACTN1, ETV7, GABBR1-MOG, MEF2C, and ZBTB9-BAK1).

211 In the absence of antibodies, IgH(MOG-mem) mice, but not mice expressing a BCR of irreleva

212 Using BM from IgH(MOG) mice that develop MOG-specific B cell receptors, we

213 We expressed mutants of MOG on human HeLa cells and analyzed sera from 111 patie

214 We prospectively studied adult patients with MOG or AQP4 antibodies who received RTX under an individ

215 dies to myelin-oligodendrocyte glycoprotein (MOG) or the glycine receptor alpha1 subunit (GlyR) is un

216 during the initial CNS inflammatory phase of MOG peptide EAE, reduces the acute and long-term severit

217 for MIF that was strongly potentiated by the MOG peptide extension, resulting in a novel therapeutic,

218 cross-reactivity of OT-1 CD8(+) T cells with MOG peptide in the CNS did not result in clinically or s

219 zation of mice lacking Orai1 in T cells with MOG peptide resulted in attenuated severity of experimen

220 oligodendrocyte glycoprotein peptide 35-55 (MOG peptide), a model of MS, documented continued axon l

221 ion of TCRs with lower affinity for the self-MOG peptide.

222 ed with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 (p35-55) for EAE induction and treate

223 3-interacting region motif of immunodominant MOG peptides abrogated their degradation.

224 The Mog phenotype is caused by ectopic expression of fog-3,

225 resulting in a masculinization of germline (Mog) phenotype.

226 l demyelinating syndromes (7 cases, all anti-MOG positive).

227 atible with demyelination (5 AQ4 positive, 2 MOG positive).

228 idation of methane (AOM) and methanogenesis (MOG) primarily occur at the depth of the sulfate-methane

229 In conclusion, EBV infection switches MOG processing in B cells from destructive to productive

230 m any numerical data; or explore an existing MOG project.

231 A researcher can create new MOG projects from any numerical data; or explore an exis

232 MOG projects, with history of explorations, can be saved

233 ncoding myelin oligodendrocyte glycoprotein (MOG) promotes disease resistance and CD4(+) T cell delet

234 Although human MOG protein was degraded less in EBV-infected than in un

235 (35-55) or the full-length recombinant human MOG protein, the latter representing the most-used B cel

236 tein (MOG) fused to reovirus protein sigma1 (MOG-psigma1), which activates Tregs, restoring protectio

237 E's pathogenesis, treatment of EAE mice with MOG-psigma1, but not OVA-psigma1, resulted in an influx

238 MOG-psigma1-, but not OVA-psigma1-induced IL-10-producin

239 ve disease, whereas the adoptive transfer of MOG-psigma1-induced B220(+)CD5(+) Bregs greatly ameliora

240 h fewer Tregs, but upon adoptive transfer of MOG-psigma1-induced BTLA(+) Bregs, BTLA(-/-) mice were p

241 ptive transfer of B220(+)CD5(-) B cells from MOG-psigma1-treated EAE or Bregs from PBS-treated EAE mi

242 methanogenic substrates as well as the high MOG rates from methylated compounds indicated that methy

243 vaccines, indicating that their loss of anti-MOG reactivity did not reflect a general lack of capacit

244 ors for myelin oligodendrocyte glycoprotein (MOG) (referred to as 2D2xTH mice), and demonstrated that

245 campus is also involved in the production of MOGs remains currently unknown.

246 The increased encephalitogenic MOG-restricted CD4(+) T cells were due to an autocrine e

247 Deletion of MOG results in aberrant sprouting of nociceptive neurons

248 drocyte glycoprotein MOG35-55 peptide (GMCSF-MOG) reversed established paralytic disease in both pass

249 esistant to EAE induced by recombinant human MOG (rhMOG), a T cell- and B cell-dependent autoantigen,

250 histone modification and gene expression in MOG sensitized lymphocytes.

251 tosidase scFv:MOG fusion protein (scFv GL117:MOG) served as isotype control.

252 refore, myelin oligodendrocyte glycoprotein (MOG)-specific autoantibodies can initiate disease bouts

253 ed number, but not function, of autoantigen (MOG)-specific pathogenic CD4 T cells in the CNS during d

254 um from Myelin oligodendrocyte glycoprotein (MOG)-specific T cell receptor-positive (TCR+) transgenic

255 CNS and myelin oligodendrocyte glycoprotein (MOG)-specific T cells in lymphoid organs.

256 o prime myelin oligodendrocyte glycoprotein (MOG)-specific Th cells compared with Ppard (fl/fl) count

257 ere are myelin oligodendrocyte glycoprotein (MOG)--specific Tregs that infiltrate into the CNS.

258 fic B cells, but not the addition of soluble MOG-specific Ab, is sufficient to drive EAE in mice expr

259 Using BM from IgH(MOG) mice that develop MOG-specific B cell receptors, we generated mixed chimer

260 As a consequence, MOG-specific B cells get help from hemagglutinin-specifi

261 cells was abrogated, resulting in a lack of MOG-specific B cells in all B cell compartments examined

262 In vivo, the transfer of MOG-specific B cells into recipient mice after the cocap

263 live and fixed cell microscopy, we show that MOG-specific B cells take up large amounts of MOG from c

264 arget cell, it can be cocaptured with MOG by MOG-specific B cells via the B-cell receptor.

265 In these animals, the development of MOG-specific B cells was abrogated, resulting in a lack

266 rther, increasing the precursor frequency of MOG-specific B cells, but not the addition of soluble MO

267 nin as a model viral antigen and transgenic, MOG-specific B cells.

268 ation, and their suppression/cytotoxicity of MOG-specific CD4 T cells is observed both in the periphe

269 is and displayed compromised reactivation of MOG-specific CD4(+) T cells in the CNS, despite elicitin

270 disease by suppressing the proliferation of MOG-specific CD4(+) T cells.

271 pecific lymphocytes and induced apoptosis of MOG-specific CD4+ T cells in a dose- and time-dependent

272 s, this was reversed by adoptive transfer of MOG-specific CD8 T cells.

273 of lower affinity T cells that comprise the MOG-specific conventional T cell (Tconv) and Treg respon

274 s showed that kirenol inhibited viability of MOG-specific lymphocytes and induced apoptosis of MOG-sp

275 ll effectors are associated with the loss of MOG-specific naive precursors.

276 Here, we report identification of a MOG-specific Qa-1 epitope.

277 ligand 1 during the initial interaction with MOG-specific T cells and used this inhibitory molecule t

278 These inflammatory DC presented MOG35-55 to MOG-specific T cells by an inhibitory mechanism that was

279 We show that MOG-specific T cells in Rras2(-/-) mice have reduced aff

280 litogenicity and expansion of high-affinity, MOG-specific T cells that defined the polyclonal respons

281 deletion of Orai1 in adoptively transferred, MOG-specific T cells was able to halt EAE progression af

282 Despite reported cross-reactivity with MOG-specific T cells, the polyclonal response to NFM15-3

283 old level of encephalitogenic, high-affinity MOG-specific T cells.

284 n blood and secondary lymphoid organs in 2D2 MOG-specific transgenic mice, and repeated boosters faci

285 Most of the MOG-specific Tregs in the CNS possessed the methylation

286 ex vivo, we demonstrate that at peak disease MOG-specific Tregs were progressively enriched in the dr

287 pinal fluid (CSF)-, MRI studies, outcome and MOG status of 33 paediatric ADEM prospectively studied w

288 ies revealed that the GM-CSF domain of GMCSF-MOG stimulated growth and differentiation of inflammator

289 we used myelin oligodendrocyte glycoprotein (MOG) T-cell receptor transgenic (2D2) mice where >80% of

290 Critically, transfer of MOG-TCR transgenic (2D2) CD4 T cells after, but not befo

291 opes in myelin oligodendrocyte glycoprotein (MOG that is a protein in myelin sheath).

292 mationally sensitive determinant on DRalpha1-MOG that is responsible for optimal binding to CD74 and

293 LP) and myelin oligodendrocyte glycoprotein (MOG), the membrane proteins found in the myelin sheath.

294 ides an overview of the current knowledge of MOG, the metrics of MOG-Ab assays and the clinical assoc

295 Genetic defects in MOGS, the gene encoding mannosyl-oligosaccharide glucosi

296 thermore, NFM lacked functional synergy with MOG to promote experimental autoimmune encephalomyelitis

297 ge (the lexical route), while lesion to left MOG was associated with errors to the phonological (non-

298 4), and myelin oligodendrocyte glycoprotein (MOG) was performed using brain immunohistochemistry and

299 human anti-MOG Abs did not recognize rodent MOG, which has implications for animal studies.

300 The interaction of MOG with DC-SIGN in the context of simultaneous TLR4 act