ライフサイエンスコーパス: MOG

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

2 MOG antibody disease spontaneously separated from multip

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

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

5 MOG-Ab-positive patients more frequently presented with

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

7 MOG-IgG serostatus was longitudinally assessed in seropo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 Furthermore, immune tolerization against MOG ameliorated symptoms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 = 40.9-86.5) of nonrelapsing children became MOG-Ab negative compared to 14.1% (95% CI = 4.7-38.3) of

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

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

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

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

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

54 The overlap between MOG antibody oligodendrocytopathy and AQP4 antibody astr

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

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

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

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

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

60 When applying scFv DEC:MOG to mice that had already experienced EAE symptoms, a

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

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

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

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

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

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

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

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

69 ted mixed chimeras together with BM-encoding MOG.

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

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

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

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

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

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

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

77 tiary centres in Spain were investigated for MOG antibodies.

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

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

80 CNS inflammatory diseases were positive for MOG-IgG.

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

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

83 4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 ng from myelin oligodendrocyte glycoprotein (MOG) immunization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 0-48 of myelin oligodendrocyte glycoprotein (MOG).

132 antigen myelin oligodendrocyte glycoprotein (MOG).

133 -191 or myelin oligodendrocyte glycoprotein (MOG)35-55 in proteolipid protein- and MOG-induced models

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

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

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

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

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

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

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

141 GMCSF-MOG also retained dominant inhibitory activity when dire

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

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

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

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

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

147 116 patients had MOG antibodies, including 94 (39%) from cohort A and 22

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

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

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

151 ation of C57BL/6 mice with recombinant human MOG (hMOG) results in experimental autoimmune encephalom

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

153 (35-55) or the full-length recombinant human MOG protein, the latter representing the most-used B cel

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

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

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

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

158 ollicle-like structures were observed in IgH(MOG-mem) mice crossed with MOG-specific TCR Tg mice.

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

160 3-interacting region motif of immunodominant MOG peptides abrogated their degradation.

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

162 histone modification and gene expression in MOG sensitized lymphocytes.

163 st 3-fold elevation in serum pNF-H levels in MOG+ mice relative to MOG-littermates (P = 0.02).

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

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

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

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

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

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

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

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

172 Interestingly, MOG-specific CD8 T cells could also suppress adoptively

173 Internalized MOG colocalized with autophagosomes, which can protect f

174 ental autoimmune encephalomyelitis involving MOG-specific, demyelinating Abs.

175 7/BL6 mice were immunized with the Hooke lab MOG kit, sacrificed at the peak of the disease and their

176 ical outcome in contrast to children lacking MOG antibodies.

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

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

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

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

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

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

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

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

185 Administration of MOG-specific antibodies only partially restored EAE susc

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

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

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

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

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

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

192 Deletion of MOG results in aberrant sprouting of nociceptive neurons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 ated at loops connecting the beta strands of MOG.

218 Thus, these data indicate that targeting of MOG to "steady-state" DCs in vivo may provide a tool to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 serum pNF-H levels in MOG+ mice relative to MOG-littermates (P = 0.02).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 tibodies were observed only in children with MOG antibodies.

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

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

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

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

276 , 2 (4%) had AQP4 antibodies concurrent with MOG antibodies, and 5 (10%) were seronegative.

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

278 e observed in IgH(MOG-mem) mice crossed with MOG-specific TCR Tg mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

294 15-35 is immunogenic and cross-reactive with MOG at the polyclonal level, it fails to expand a thresh

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

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

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

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

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

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