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(97-109)-reactive CD4(+) T cells, isolated with DRB1*

4 MOG+ mice with the lowest PERG amplitudes had optic nerv

5 MOG-Ab-positive patients more frequently presented with

6 MOG-IgG serostatus was longitudinally assessed in seropo

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

8 MOG-specific T-cells also trafficked less efficiently to

9 MOG-stimulated splenocytes from these mice showed elevat

10 clones from single cell cloning of DRB1*0401/MOG(97-109(107E-S)) tetramer(+) cells confirmed that the

11 their frequency was measured using DRB1*0401/MOG(97-109(107E-S)) tetramers in MS subjects and healthy

12 tive CD4(+) T cells, isolated with DRB1*0401/MOG(97-109) tetramers, and after a short-term culture of

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

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

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

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

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

18 oligodendrocyte glycoprotein peptide 35-55 (MOG-peptide), nor were there significant differences bet

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

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

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

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

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

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

25 Furthermore, immune tolerization against MOG ameliorated symptoms.

26 day 10 (prior to behavioral symptoms) in all MOG-injected groups, ii) a significant reduction of acti

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

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

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

30 Moreover, NPs carrying ITE and MOG(35-55) expanded the FoxP3(+) Treg compartment and su

31 ction of activated astrocytes in MOG+OGF and MOG+LDN groups compared to MOG+Vehicle mice at day 30, a

32 - and 3-fold more animals in the MOG+OGF and MOG+LDN groups, respectively, had a remission compared t

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

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

35 -beta secretion by myelin basic protein- and MOG-peptide-specific T cells, as well as ex vivo isolate

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

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

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

39 , as well as a significant reduction in anti-MOG Ab and splenocyte proliferation to MOG.

40 e central nervous system, and increased anti-MOG antibody and proinflammatory cytokine production, es

41 roduction associated with ART increased anti-MOG antibody titers, as well as B-cell survival factor B

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

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

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

45 In half of the patients, the anti-MOG response was directed to a single epitope.

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

47 therefore informative for understanding anti-MOG humoral responses in MS.

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

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

50 g the recognition of the myelin autoantigen, MOG(35-55).

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

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

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

54 The overlap between MOG antibody oligodendrocytopathy and AQP4 antibody astr

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

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

57 rotein had a higher amount of conformational MOG antibodies present in serum.

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 oligodendrocyte glycoprotein (MOG; scFv DEC:MOG).

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

63 Furthermore, DCs isolated from scFv DEC:MOG-injected animals produced significantly increased le

64 mportantly, when EAE was induced in scFv DEC:MOG-injected mice, 90% of the mice were protected from E

65 ty both by generating conformation-dependent MOG antibodies and by enhancing its processing or/and pr

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

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

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

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

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

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

72 -cell responses against the encephalitogenic MOG 91-108 epitope were greatly enhanced after refolding

73 ted mixed chimeras together with BM-encoding MOG.

74 ein in vitro, suggesting that the endogenous MOG protein was not processed to the MOG(35-55) peptide

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

76 e used MOG peptides or bacterially expressed MOG, neither of which contain the tertiary structure of

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

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

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

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

81 CNS inflammatory diseases were positive for MOG-IgG.

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

83 rossed with mice bearing an IgH specific for MOG, the mice develop spontaneous EAE with high incidenc

84 4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

85 GILT APCs could not generate MOG(35-55) from MOG protein in vitro, suggesting that the endogenous MOG

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

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

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

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 GILT(-/-) mice, GILT APCs could not generate MOG(35-55) from MOG protein in vitro, suggesting that th

92 all mice in the isotype controls (scFv GL117:MOG) experienced development of EAE.

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

94 signs in myelin oligodendrocyte glycoprotein MOG(35-55)- induced experimental allergic encephalomyeli

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

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

97 ns of a myelin oligodendrocyte glycoprotein (MOG) 35-55-reactive TCR (1C6) on the NOD background.

98 fic for myelin oligodendrocyte glycoprotein (MOG) and lymphocytic choriomeningitis virus (LCMV) antig

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

100 Anti-myelin-oligodendrocyte glycoprotein (MOG) antibody production, interleukin (IL)-4, IL-8, IL-1

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

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

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

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

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

106 opes of myelin oligodendrocyte glycoprotein (MOG) have a demyelinating potential in the animal model

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

108 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experi

109 ng from myelin oligodendrocyte glycoprotein (MOG) immunization.

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

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

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

113 rity of myelin oligodendrocyte glycoprotein (MOG) peptide-induced experimental autoimmune encephalomy

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

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

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

117 pe from myelin oligodendrocyte glycoprotein (MOG)(35)(-55) to promote the generation of Tregs by DCs.

118 severe myelin oligodendrocyte glycoprotein (MOG)(35\x{2013}55)-induced experimental allergic encepha

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

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

121 istered myelin oligodendrocyte glycoprotein (MOG), which contains disulfide bonds, to generate experi

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

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

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

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

126 rity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE when administered after disease onset.

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

128 able to myelin oligodendrocyte glycoprotein (MOG)-induced EAE, with a severe, nonresolving atypical f

129 sion of myelin oligodendrocyte glycoprotein (MOG)-induced EAE.

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

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

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

133 ess the myelin oligodendrocyte glycoprotein (MOG)-specific B cell receptor (BCR; IgH(MOG-mem)) but ca

134 CR6 and myelin oligodendrocyte glycoprotein (MOG)-specific CD4(+) T cells accumulated within the chem

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

136 whether myelin oligodendrocyte glycoprotein (MOG)-specific T cells could be detected and their freque

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

138 CD137L, myelin oligodendrocyte glycoprotein (MOG)-specific T-cells secreted lower levels of T(h)1/T(h

139 antigen myelin oligodendrocyte glycoprotein (MOG).

140 0-48 of myelin oligodendrocyte glycoprotein (MOG).

141 -191 or myelin oligodendrocyte glycoprotein (MOG)35-55 in proteolipid protein- and MOG-induced models

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

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

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

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

146 self-Ag myelin oligodendrocyte glycoprotein (MOG; scFv DEC:MOG).

147 [MBP], myelin-oligodendrocyte glycoprotein [MOG], beta-actin [ACTB], thymosin beta-10 [TB10], and su

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

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

150 GMCSF-MOG also retained dominant inhibitory activity when dire

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

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

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

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

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

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

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

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

159 Non-refolded recombinant human MOG does not induce EAE in DA rats.

160 DA rats immunized with refolded human MOG developed severe acute EAE.

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

162 maR(-/-) mice, uptake and presentation of Ig-MOG occurs and the animals were able to overcome experim

163 Furthermore, oral Ig-MOG was able to overcome experimental autoimmune encepha

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

165 ein (MOG)-specific B cell receptor (BCR; IgH(MOG-mem)) but cannot secrete antibodies.

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

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

168 3-interacting region motif of immunodominant MOG peptides abrogated their degradation.

169 ificant reduction of activated astrocytes in MOG+OGF and MOG+LDN groups compared to MOG+Vehicle mice

170 Kv1.3 was the only K(V) channel expressed in MOG 35-55-specific CD4(+) T cell blasts, and no K(V) cur

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

172 l blasts, and no K(V) current was present in MOG-specific CD4(+) T cell-blasts from Kv1.3 KO mice.

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

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

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

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

177 Internalized MOG colocalized with autophagosomes, which can protect f

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

179 7/BL6 mice were immunized with the Hooke lab MOG kit, sacrificed at the peak of the disease and their

180 ical outcome in contrast to children lacking MOG antibodies.

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

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

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

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

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

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

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

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

189 droglial NMDARs, did not alter the course of MOG-peptide EAE.

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

191 Deletion of MOG results in aberrant sprouting of nociceptive neurons

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

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

194 adjuvant treatment suppressed development of MOG-specific IL-17.

195 In addition to altering the distribution of MOG-specific T cells, adjuvant treatment suppressed deve

196 But in addition, a striking effect of MOG refolding on the generation of T-cell responses was

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 Thus, CD137L regulates many functions of MOG-specific T-cells that contribute to EAE and may repr

200 protein in order to assess the influence of MOG conformation on its pathogenicity in DA rats.

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

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

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

204 icant participants in the pathophysiology of MOG-peptide EAE.

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

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

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

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

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

210 Therefore, we conclude that refolding of MOG increases its pathogenicity both by generating confo

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

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

213 ated at loops connecting the beta strands of MOG.

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

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

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

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

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

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

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

221 nflammatory cytokine secretion of pathogenic MOG(35-55)-specific T-cells.

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

223 myelin oligodendrocyte glycoprotein peptide (MOG)-induced experimental autoimmune encephalomyelitis (

224 myelin oligodendrocyte glycoprotein peptide (MOG).

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

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

227 n contrast to WT rat MOG-immunized mice, rat MOG-immunized GILT(-/-) mice generated Abs that transfer

228 ced EAE but slightly more susceptible to rat MOG protein-induced EAE than wild-type (WT) mice.

229 Immunization of GILT(-/-) mice with rat MOG protein resulted in a switch in pathogenic mechanism

230 In contrast to WT rat MOG-immunized mice, rat MOG-immunized GILT(-/-) mice gen

231 oth CD4(+) and CD8(+) T cells that recognize MOG and produce proinflammatory cytokines, allowing for

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

233 otein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis af

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

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

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

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

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

239 nsive to both the native and the substituted MOG peptide.

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

241 T cells proliferated to peptides other than MOG(35-55).

242 OG(35-55) peptide would induce EAE, but that MOG protein would not.

243 We further demonstrated that MOG- and LCMV-specific CD4(+) T cells possessed similarl

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

245 One possibility was that MOG(35-55) peptide would induce EAE, but that MOG protei

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

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

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

249 By day 60, 6- and 3-fold more animals in the MOG+OGF and MOG+LDN groups, respectively, had a remissio

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

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

252 ogenous MOG protein was not processed to the MOG(35-55) peptide in vivo.

253 Even though MOG(35-55) was immunogenic in GILT(-/-) mice, GILT APCs

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

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

256 es in MOG+OGF and MOG+LDN groups compared to MOG+Vehicle mice at day 30, and iii) no demyelination on

257 s, respectively, had a remission compared to MOG+Vehicle mice.

258 ) mice generated Abs that transferred EAE to MOG(35-55)-primed GILT(-/-) mice, and these Abs bound to

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

260 anti-MOG Ab and splenocyte proliferation to MOG.

261 aring CD4(+) T cells and B cells reactive to MOG on the C57BL/6 background.

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

263 GILT(-/-) mice were relatively resistant to MOG(35-55)-induced EAE but slightly more susceptible to

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

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

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

267 ction of EAE, most studies to date have used MOG peptides or bacterially expressed MOG, neither of wh

268 ound 4 was selected to partake in an in vivo MOG EAE mouse model study to evaluate its effect in MS-l

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

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

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

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

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

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

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

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

277 tibodies were observed only in children with MOG antibodies.

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

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

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

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

282 , 2 (4%) had AQP4 antibodies concurrent with MOG antibodies, and 5 (10%) were seronegative.

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

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

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

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

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

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

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

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

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

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

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

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

295 and after a short-term culture of PMBCs with MOG(97-109) peptides, were detected more frequently from

296 15-35 is immunogenic and cross-reactive with MOG at the polyclonal level, it fails to expand a thresh

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

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

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

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

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