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1 yelin basic protein, proteolipid protein, or myelin oligodendrocyte glycoprotein.
2 ntal autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein.
3 is severity by limiting central tolerance to myelin oligodendrocyte glycoprotein.
4 myelin-specific genes (myelin basic protein, myelin oligodendrocyte glycoprotein, 2',3'-cyclic-nucleo
11 pared with that of control T cells following myelin oligodendrocyte glycoprotein 35-55 restimulation
13 diabetes, we found them more susceptible to myelin oligodendrocyte glycoprotein 35-55-induced EAE co
15 nt of young males inhibited proliferation of myelin oligodendrocyte glycoprotein 35-55-specific T cel
18 kly within the spleen, but not CNS following myelin oligodendrocyte glycoprotein(35-55) immunization,
19 dy that the generation of these effectors in myelin oligodendrocyte glycoprotein(35-55)-induced exper
21 A/IFN-gamma double reporter mouse and I-A(b)/myelin oligodendrocyte glycoprotein 38-49 tetramer, we s
22 CD8(+) T cells recognize the myelin peptide myelin oligodendrocyte glycoprotein 40-54 (MOG40-54) bot
23 experiments, we found that highly purified, myelin oligodendrocyte glycoprotein Ag-specific Th17 cel
24 on EAE induction by active immunization with myelin oligodendrocyte glycoprotein amino acids 35-55 (M
25 P4-IgG, pathogenetic serum IgG antibodies to myelin oligodendrocyte glycoprotein, an antigen in the o
26 th a sequence relationship between BTNL2 and myelin oligodendrocyte glycoprotein, an autoantigen asso
29 utaneous immunization with recombinant human myelin oligodendrocyte glycoprotein and then Ab once wee
30 e of antibodies recognizing the autoantigen, myelin oligodendrocyte glycoprotein and tumour target, H
31 d controls) by the subcutaneous injection of myelin oligodendrocyte glycoprotein, and after disease o
33 g myelin basic protein, proteolipid protein, myelin oligodendrocyte glycoprotein, and myelin-associat
34 o the host mice supports suppression of both myelin oligodendrocyte glycoprotein- and myelin basic pr
35 Foxp3 also was observed during priming with myelin oligodendrocyte glycoprotein, another target neur
36 gainst aquaporin-4 (AQP4-Abs), but recently, myelin-oligodendrocyte glycoprotein antibodies (MOG-Abs)
39 samples against four neurologic surface Ags (myelin oligodendrocyte glycoprotein, aquaporin 4, acetyl
40 elin basic protein, proteolipid protein, and myelin oligodendrocyte glycoprotein by immunostaining of
41 myelin basic protein, and to a lesser extent myelin oligodendrocyte glycoprotein, can serve as MSP su
42 chronic, nonremitting, paralytic disease in myelin oligodendrocyte glycoprotein-challenged C57BL/6 m
43 D1(G93A) mice were significantly depleted in myelin-oligodendrocyte glycoprotein compared with those
44 iously shown that the 2D2 TCR recognizes the myelin oligodendrocyte glycoprotein epitope (MOG)35-55 a
45 self-epitopes such as has been suggested for myelin oligodendrocyte glycoprotein epitope 35-55 (MOG35
46 argely confined to induction with either the myelin oligodendrocyte glycoprotein epitope MOG(35-55) o
49 E mice were given subcutaneous injections of myelin oligodendrocyte glycoprotein fragment1-125 emulsi
50 ment of PPAR-beta to the promoter of PLP and myelin oligodendrocyte glycoprotein genes in human oligo
51 autoimmune encephalomyelitis was induced by myelin-oligodendrocyte glycoprotein immunization in fema
52 ack of CNS inflammation and demyelination in myelin oligodendrocyte glycoprotein-immunized Def6(-/-)
55 une encephalomyelitis (EAE) was induced with myelin oligodendrocyte glycoprotein in humanized HLA-DR2
56 myelin-derived Ags (myelin basic protein and myelin oligodendrocyte glycoprotein) in palatine tonsils
57 CD3-specific antibody-mediated prevention of myelin oligodendrocyte glycoprotein-induced acute experi
58 D1480 treatment inhibits disease severity in myelin oligodendrocyte glycoprotein-induced classical an
59 y that deletion of the C3aR is protective in myelin oligodendrocyte glycoprotein-induced EAE in C57BL
60 d AZD8797 treatment in Dark Agouti rats with myelin oligodendrocyte glycoprotein-induced EAE resulted
62 cells that present Ag within the CNS during myelin oligodendrocyte glycoprotein-induced EAE, with th
63 ice was sufficient to reduce the severity of myelin oligodendrocyte glycoprotein-induced experimental
65 ted viral (AAV) system in the mouse model of myelin oligodendrocyte glycoprotein-induced experimental
66 ell-mediated autoimmune diseases, we studied myelin oligodendrocyte glycoprotein-induced experimental
67 ne demyelinating model of multiple sclerosis-myelin oligodendrocyte glycoprotein-induced experimental
68 also developed similar levels of disease in myelin oligodendrocyte glycoprotein-induced experimental
70 iorates neurological deficit and severity of myelin oligodendrocyte glycoprotein-induced experimental
71 use the murine model of the 35-55 peptide of myelin oligodendrocyte glycoprotein-induced experimental
73 y, the adoptive transfer of CD31-conditioned myelin oligodendrocyte glycoprotein-loaded DCs carried i
74 ) premyelinating and myelin basic protein(+)/myelin oligodendrocyte glycoprotein(+) mature oligodendr
75 ats pre-immunized with a subclinical dose of myelin oligodendrocyte glycoprotein mimicked the patholo
76 (CYM-5442) at the onset of clinical signs in myelin oligodendrocyte glycoprotein MOG(35-55)- induced
77 this question, we analyzed Qa-1 epitopes in myelin oligodendrocyte glycoprotein (MOG that is a prote
78 ncreased Th17 cell polarization in vivo upon myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide
79 Here, we subjected PACAP-deficient mice to myelin oligodendrocyte glycoprotein (MOG(35-55))-induced
81 ll activation, and promote the generation of myelin oligodendrocyte glycoprotein (MOG(35-55))-specifi
83 hich T and B cells overexpress receptors for myelin oligodendrocyte glycoprotein (MOG) (referred to a
86 at expresses the alpha- and beta-chains of a myelin oligodendrocyte glycoprotein (MOG) 35-55-reactive
87 n this study, we demonstrate that individual myelin oligodendrocyte glycoprotein (MOG) 35-55-specific
88 f CD43 also affected cytokine production, as myelin oligodendrocyte glycoprotein (MOG) 35-55-specific
89 istry for two strongly down-regulated genes, myelin oligodendrocyte glycoprotein (Mog) and ermin (Erm
90 ctive CD4(+) T cell populations specific for myelin oligodendrocyte glycoprotein (MOG) and lymphocyti
94 mpare clinical features, disease course, and myelin oligodendrocyte glycoprotein (MOG) antibody (Ab)
97 antibodies targeting conformationally intact myelin oligodendrocyte glycoprotein (MOG) are found in d
99 on of antibodies against folded or denatured myelin oligodendrocyte glycoprotein (MOG) by selective u
102 with the extracellular Ig-like domain of rat myelin oligodendrocyte glycoprotein (MOG) developed expe
103 injected i.v. with an autoantigen peptide of myelin oligodendrocyte glycoprotein (MOG) developed less
104 otect a proteolysis-sensitive immunodominant myelin oligodendrocyte glycoprotein (MOG) epitope (resid
105 encephalomyelitis (EAE) can be achieved with myelin oligodendrocyte glycoprotein (MOG) fused to reovi
106 cognizing conformation-dependent epitopes of myelin oligodendrocyte glycoprotein (MOG) have a demyeli
108 -FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization c
110 cells to enhance EAE severity resulting from myelin oligodendrocyte glycoprotein (MOG) immunization.
117 ion of C57BL/6 mice with either rat or human myelin oligodendrocyte glycoprotein (MOG) leads to exper
118 ype littermates, following immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 peptide
120 or C57BL/6NOS2(-/)- mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55
121 et and a more chronic form of EAE induced by myelin oligodendrocyte glycoprotein (MOG) peptide 35-55
122 ficient (Nrf2(-/-)) mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55
124 nd that PKC theta-/- mice immunized with the myelin oligodendrocyte glycoprotein (MOG) peptide MOG(35
125 ignificantly lower incidence and severity of myelin oligodendrocyte glycoprotein (MOG) peptide-induce
128 row (BM) transduced with retrovirus encoding myelin oligodendrocyte glycoprotein (MOG) promotes disea
132 ergic encephalomyelitis when treated with Ig-myelin oligodendrocyte glycoprotein (MOG) tolerogen, an
133 antibodies to NMDAR, aquaporin-4 (AQP4), and myelin oligodendrocyte glycoprotein (MOG) was performed
136 zation of C57BL/6 mice with the neuroantigen myelin oligodendrocyte glycoprotein (MOG) with CFA, whic
137 o coadminister ITE and a T-cell epitope from myelin oligodendrocyte glycoprotein (MOG)(35)(-55) to pr
138 y (EAE) induced by immunization of mice with myelin oligodendrocyte glycoprotein (MOG)(35-55) Ig-like
139 he AhR agonist ITE and a T cell epitope from myelin oligodendrocyte glycoprotein (MOG)(35-55) induced
140 EAE, both mouse strains were sensitized with myelin oligodendrocyte glycoprotein (MOG)(35-55) peptide
142 ), yet IFN-gamma production is comparable to myelin oligodendrocyte glycoprotein (MOG)(35-55)-immuniz
144 ped Foxp3gfp knock-in (Foxp3gfp.KI) mice and myelin oligodendrocyte glycoprotein (MOG)(35-55)/IA(b) (
145 disrupted Hrh4 (H(4)RKO) develop more severe myelin oligodendrocyte glycoprotein (MOG)(35\x{2013}55)-
148 t are deficient in miR-146a and specific for myelin oligodendrocyte glycoprotein (MOG), an autoantige
150 iredoxin 4 (Prdx4), stathmin-like 2 (Stmn2), myelin oligodendrocyte glycoprotein (MOG), and versican
151 tein levels of proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), the membrane
152 mice would process exogenously administered myelin oligodendrocyte glycoprotein (MOG), which contain
153 D-CM) inhibited the proliferation of murine myelin oligodendrocyte glycoprotein (MOG)-(35-55)-specif
154 ental autoimmune encephalomyelitis there are myelin oligodendrocyte glycoprotein (MOG)--specific Treg
155 In a previous study, we demonstrated that myelin oligodendrocyte glycoprotein (MOG)-35-55 peptide
156 severity than males after immunization with myelin oligodendrocyte glycoprotein (MOG)-35-55 peptide/
157 SD patients and also assessed their value in myelin oligodendrocyte glycoprotein (MOG)-ab positive an
159 Ab-seropositive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositiv
160 n using histological methods in chronic EAE [myelin oligodendrocyte glycoprotein (MOG)-induced diseas
161 lls diminishes the intensity and duration of myelin oligodendrocyte glycoprotein (MOG)-induced EAE an
162 (2) treatment diminishes progression of both myelin oligodendrocyte glycoprotein (MOG)-induced EAE in
163 nses and attenuates the clinical severity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE wh
164 GAS6 directly into the CNS of WT mice during myelin oligodendrocyte glycoprotein (MOG)-induced EAE wo
165 cific SOCS3-deficient mice are vulnerable to myelin oligodendrocyte glycoprotein (MOG)-induced EAE, w
166 Rbeta1(-/-) mice are completely resistant to myelin oligodendrocyte glycoprotein (MOG)-induced EAE, w
167 antagonist naltrexone (LDN) on expression of myelin oligodendrocyte glycoprotein (MOG)-induced EAE.
168 matory bowel disease (IBD) and in a model of myelin oligodendrocyte glycoprotein (MOG)-induced experi
169 he central nervous system (CNS) of mice with myelin oligodendrocyte glycoprotein (MOG)-induced experi
170 's murine encephalomyelitis virus (TMEV) and myelin oligodendrocyte glycoprotein (MOG)-induced experi
171 tested the consequences of AhR activation in myelin oligodendrocyte glycoprotein (MOG)-induced experi
172 of Hrd1 function in DCs protected mice from myelin oligodendrocyte glycoprotein (MOG)-induced experi
173 -17, IL-6, IFN-gamma, and TNF-alpha, and the myelin oligodendrocyte glycoprotein (MOG)-induced IL-17,
176 reated transgenic (Tg) mice that express the myelin oligodendrocyte glycoprotein (MOG)-specific B cel
177 nate chemokine receptors CXCR3 and CXCR6 and myelin oligodendrocyte glycoprotein (MOG)-specific CD4(+
178 repeated antigenic stimulation of pathogenic myelin oligodendrocyte glycoprotein (MOG)-specific CD4(+
179 ne disease using the CD4(+) T cell-dependent myelin oligodendrocyte glycoprotein (MOG)-specific exper
181 ased numbers of T lymphocytes in the CNS and myelin oligodendrocyte glycoprotein (MOG)-specific T cel
184 /fl) mice had a heightened capacity to prime myelin oligodendrocyte glycoprotein (MOG)-specific Th ce
188 for the tolerogenic vaccine Ag PLP178-191 or myelin oligodendrocyte glycoprotein (MOG)35-55 in proteo
189 (-/-) mice showed enhanced susceptibility to myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-i
190 ely ameliorated clinical disease severity in myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-i
192 lomyelitis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide.
193 esistant to EAE induced by immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 The mecha
194 responses to PLP139-151, but not PLP178-191, myelin oligodendrocyte glycoprotein (MOG)35-55, or OVA32
195 M knockout (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG)35-55-induced e
196 contribution of CD4(+) and CD8(+) T cells in myelin oligodendrocyte glycoprotein (MOG)35-55-induced E
197 for DEC205 and fused the scFv to the self-Ag myelin oligodendrocyte glycoprotein (MOG; scFv DEC:MOG).
198 of ON in C57BL/6 (B6) mice immunized with a myelin oligodendrocyte/glycoprotein (MOG)-derived peptid
200 ns at 90 and 180 days post-EAE induction via myelin-oligodendrocyte glycoprotein (MOG) injection.
201 l setting, the significance of antibodies to myelin-oligodendrocyte glycoprotein (MOG) or the glycine
202 ays (CBA) for aquaporin-4 (AQP4)-M23-IgG and myelin-oligodendrocyte glycoprotein (MOG)-alpha1-IgG.
204 ogical disorders with IgG antibodies against myelin-oligodendrocyte glycoprotein (MOG-IgG) have been
206 enhanced by addition of a peptide extension (myelin oligodendrocyte glycoprotein [MOG]-35-55 peptide)
207 to induce allogenic as well as Ag-specific (myelin oligodendrocyte glycoprotein [MOG]35-55) T cell r
208 n schizophrenia (myelin basic protein [MBP], myelin-oligodendrocyte glycoprotein [MOG], beta-actin [A
210 addressed the functional role of TIMP-1 in a myelin oligodendrocyte glycoprotein (MOG35-55)-induced m
211 TCR beta-chain knockout (KO) recipients of a myelin oligodendrocyte glycoprotein p35-55 encephalitoge
215 ined the effect of global CD44 deficiency on myelin oligodendrocyte glycoprotein peptide (MOG)-induce
217 d by active immunization with 100 micro g of myelin oligodendrocyte glycoprotein peptide (MOG)p35-55.
218 clinical symptoms of EAE induced in mice by myelin oligodendrocyte glycoprotein peptide (MOG35-55) i
220 encephalomyelitis (EAE) by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG p
221 induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG p
222 licited in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG-p
223 present study we show that immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35
224 mmune encephalomyelitis (EAE), induced using myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35
225 e to EAE induced with a peptide derived from myelin oligodendrocyte glycoprotein peptide 35-55 (MOGp3
226 d WY14,643 display impaired IgG responses to myelin oligodendrocyte glycoprotein peptide 35-55 (pMOG(
227 cytokine secretion of T cells to the self Ag myelin oligodendrocyte glycoprotein peptide 35-55 and to
229 before induction of EAE with a neuroantigen, myelin oligodendrocyte glycoprotein peptide 35-55, and a
230 6 mice with EAE induced by immunization with myelin oligodendrocyte glycoprotein peptide 35-55, the f
231 h wild-type mice following immunization with myelin oligodendrocyte glycoprotein peptide 35-55, while
236 ronic disease in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein peptide and of relap
238 T cells following immunization of mice with myelin oligodendrocyte glycoprotein peptide in complete
239 rom IFN-alpha-treated mice re-exposed to the myelin oligodendrocyte glycoprotein peptide in vitro sho
240 ion of CD44(+) encephalitogenic T cells with myelin oligodendrocyte glycoprotein peptide led to demet
241 14, 21 or 35 days after vaccination with the myelin oligodendrocyte glycoprotein peptide MOG(35-55).
242 ugh the use of primary immunization with the myelin oligodendrocyte glycoprotein peptide to induce ex
243 se, adoptive transfer of B cells pulsed with myelin oligodendrocyte glycoprotein peptide(35-55) (MOGp
244 mponent in C activation, is not essential in myelin oligodendrocyte glycoprotein peptide-induced EAE
245 te that targeted deletion of CD44 attenuated myelin oligodendrocyte glycoprotein peptide-induced expe
246 ) to explore these issues in adult mice with myelin oligodendrocyte glycoprotein peptide-induced expe
247 e, the mice were significantly less prone to myelin oligodendrocyte glycoprotein peptide-induced expe
253 we report that synthetic peptides 35-55 from myelin oligodendrocyte glycoprotein (pMOG(35-55)) consis
254 majority of CNS-infiltrating CD4 T cells are myelin oligodendrocyte glycoprotein reactive at all time
255 highest affinity and frequency of polyclonal myelin oligodendrocyte glycoprotein-reactive cells infil
256 cient mice, showing a profound defect in the myelin oligodendrocyte glycoprotein-reactive T cell popu
257 a and interleukin-4 production by pathogenic myelin oligodendrocyte glycoprotein-reactive T cells.
258 f encephalitogenic cytokines by the targeted myelin oligodendrocyte glycoprotein-reactive T-cells but
259 eeding low doses of 0.5 mg OVA or 250 microg myelin oligodendrocyte glycoprotein resulted in up-regul
260 utaneous immunization with recombinant human myelin oligodendrocyte glycoprotein (rhMOG) in CFA on da
263 spontaneous autoimmune CNS demyelination in myelin oligodendrocyte glycoprotein-specific 2D2 TCR tra
264 ally elevated plasma cell numbers and higher myelin oligodendrocyte glycoprotein-specific Ab levels d
266 o suppress IFN-gamma and IL-17 production by myelin oligodendrocyte glycoprotein-specific CD4(+) T ce
268 deficiency resulted in a severely diminished myelin oligodendrocyte glycoprotein-specific CD4+ T cell
269 28+ T cells suppress IFN-gamma production of myelin oligodendrocyte glycoprotein-specific CD4+ T cell
270 vivo, we cotransferred these antibodies with myelin oligodendrocyte glycoprotein-specific encephalito
271 lso applicable in autoimmune disease because myelin oligodendrocyte glycoprotein-specific Foxp3(+) T
272 s a significant decrease in the frequency of myelin oligodendrocyte glycoprotein-specific IFN-gamma-p
273 induced protection of EAE and suppression of myelin oligodendrocyte glycoprotein-specific IL-17(+)CD4
274 d B cells as well as increased production of myelin oligodendrocyte glycoprotein-specific IL-17, IFN-
275 show that CD4(+)CD25(+)LAP(+) cells suppress myelin oligodendrocyte glycoprotein-specific immune resp
280 served when Tob1(-)/(-) mice were crossed to myelin oligodendrocyte glycoprotein-specific T cell rece
281 rvival; accordingly, ASC(-/-) mice had fewer myelin oligodendrocyte glycoprotein-specific T cells in
282 study, we showed that highly purified CD8(+) myelin oligodendrocyte glycoprotein-specific T cells ind
283 ctionally, SOCS-3-transduced DCs drove naive myelin oligodendrocyte glycoprotein-specific T cells to
284 n the CNS during EAE, are highly enriched in myelin oligodendrocyte glycoprotein-specific T cells.
285 D4-Cre and crossed these with mice bearing a myelin oligodendrocyte glycoprotein-specific TCR transge
286 led to induce EAE after adoptive transfer of myelin oligodendrocyte glycoprotein-specific TCR-transge
290 ere, we have developed protocols to generate myelin oligodendrocyte glycoprotein-specific Th17, Th1,
291 lso enhanced their costimulatory activity to myelin oligodendrocyte glycoprotein-specific, TCR-transg
292 ls from C57BL/6J mice activated in vivo with myelin oligodendrocyte glycoprotein, Staphylococcal ente
293 ntral nervous system (CNS)-specific antigen, myelin oligodendrocyte glycoprotein, that usually develo
294 in oral tolerance we fed low doses of OVA or myelin oligodendrocyte glycoprotein to B cell-deficient
295 , presentation to primary T cells of OVA and myelin oligodendrocyte glycoprotein, two Ags that contai
296 eration in vivo, we targeted a self antigen, myelin oligodendrocyte glycoprotein, using antibodies ag
297 ainst aquaporin 4 and high-titer Abs against myelin oligodendrocyte glycoprotein were, as expected, s
298 , such as proteolipid protein, MAG, MBP, and myelin oligodendrocyte glycoprotein, were rapidly downre
299 another oligodendrocyte-specific component, myelin oligodendrocyte glycoprotein, which is expressed
300 ate antigens such as myelin basic protein or myelin-oligodendrocyte glycoprotein, with inconclusive r