ライフサイエンスコーパス: MOG

1 antigen myelin oligodendrocyte glycoprotein (MOG).

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

3 oligodendrocyte glycoprotein (MOG; scFv DEC:MOG).

4 0-48 of myelin oligodendrocyte glycoprotein (MOG).

5 ted mixed chimeras together with BM-encoding MOG.

6 ated at loops connecting the beta strands of MOG.

7 anti-MOG Ab and splenocyte proliferation to MOG.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 -191 or myelin oligodendrocyte glycoprotein (MOG)35-55 in proteolipid protein- and MOG-induced models

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 MOG-Ab-positive patients more frequently presented with

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

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

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

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

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

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

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

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

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

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

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

58 4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

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

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

61 GMCSF-MOG also retained dominant inhibitory activity when dire

62 Furthermore, immune tolerization against MOG ameliorated symptoms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 , 2 (4%) had AQP4 antibodies concurrent with MOG antibodies, and 5 (10%) were seronegative.

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

89 ical outcome in contrast to children lacking MOG antibodies.

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

91 tibodies were observed only in children with MOG antibodies.

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

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

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

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

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

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

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

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

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

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

102 MOG antibody disease spontaneously separated from multip

103 The overlap between MOG antibody oligodendrocytopathy and AQP4 antibody astr

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

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

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

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

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

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

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

111 15-35 is immunogenic and cross-reactive with MOG at the polyclonal level, it fails to expand a thresh

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

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

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

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

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

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

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

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

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

121 Internalized MOG colocalized with autophagosomes, which can protect f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 MOG-IgG serostatus was longitudinally assessed in seropo

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

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

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

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

152 CNS inflammatory diseases were positive for MOG-IgG.

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

154 ng from myelin oligodendrocyte glycoprotein (MOG) immunization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 MOGS is expressed in the endoplasmic reticulum and is in

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

183 7/BL6 mice were immunized with the Hooke lab MOG kit, sacrificed at the peak of the disease and their

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

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

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

187 6 and 11 years, with MOGS-CDG and biallelic MOGS (mannosyl-oligosaccharide glucosidase) mutations (G

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 3-interacting region motif of immunodominant MOG peptides abrogated their degradation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Deletion of MOG results in aberrant sprouting of nociceptive neurons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 MOG-stimulated splenocytes from these mice showed elevat

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

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

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

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

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

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

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

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

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

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

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

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

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

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