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1 specific suppression of ongoing experimental allergic encephalomyelitis.
2 and its principal animal model, experimental allergic encephalomyelitis.
3 that confers resistance against experimental allergic encephalomyelitis.
4 o appropriately resolve induced experimental allergic encephalomyelitis.
5 autoimmune encephalomyelitis or experimental allergic encephalomyelitis.
6 protection of the mice against experimental allergic encephalomyelitis.
7 immunity and protection against experimental allergic encephalomyelitis.
8 nesis of multiple sclerosis and experimental allergic encephalomyelitis.
9 immune-mediated illness such as experimental allergic encephalomyelitis.
10 ible to the active induction of experimental allergic encephalomyelitis.
11 , and amyloidosis and mice with experimental allergic encephalomyelitis.
12 model of MS, chronic relapsing experimental allergic encephalomyelitis.
13 chanism for the pathogenesis of experimental allergic encephalomyelitis.
14 multiple sclerosis and the marmoset model of allergic encephalomyelitis.
15 uestion the Th1-Th2 paradigm in experimental allergic encephalomyelitis.
16 n-reactive T cells and modulate experimental allergic encephalomyelitis.
17 ted autoimmune diseases such as experimental allergic encephalomyelitis.
18 r cells capable of transferring experimental allergic encephalomyelitis.
19 ein (MOG)(35\x{2013}55)-induced experimental allergic encephalomyelitis.
20 e animals were able to overcome experimental allergic encephalomyelitis.
21 lly interconvert respond during experimental allergic encephalomyelitis.
22 evere disease manifestations in experimental allergic encephalomyelitis.
23 ediated protection of Tregs and experimental allergic encephalomyelitis.
24 that confers resistance against experimental allergic encephalomyelitis.
25 ing a model autoimmune disease, experimental allergic encephalomyelitis.
26 IMP1 promotes neuropathology in experimental allergic encephalomyelitis.
27 h less severe acute early-phase experimental allergic encephalomyelitis.
28 vo effects of tyrphostin B42 in experimental allergic encephalomyelitis, a Th1 cell-mediated autoimmu
29 n their Point of View entitled "Experimental Allergic Encephalomyelitis: A Misleading Model of Multip
30 specific suppression of ongoing experimental allergic encephalomyelitis (an MS animal model), and the
31 meliorated adoptive transfer of experimental allergic encephalomyelitis, an animal model of MS, via T
32 eat chronic relapsing-remitting experimental allergic encephalomyelitis, an animal model of multiple
33 were effective in treatment of experimental allergic encephalomyelitis, an animal model of multiple
34 es Tregs and protects mice from experimental allergic encephalomyelitis, an animal model of multiple
35 e for oligodendrocytes (OLG) in experimental allergic encephalomyelitis, an animal model of multiple
36 al and pathological features of experimental allergic encephalomyelitis, an animal model of multiple
39 meliorated clinical severity of experimental allergic encephalomyelitis, an effect that partially inv
40 red autoimmune disease locus in experimental allergic encephalomyelitis and experimental allergic orc
41 ector memory T (T(EM)) cells in experimental allergic encephalomyelitis and in myelin-specific T cell
42 ffective both in suppression of experimental allergic encephalomyelitis and in the treatment of relap
43 ffective both in suppression of experimental allergic encephalomyelitis and in the treatment of relap
47 ggest that its effectiveness in experimental allergic encephalomyelitis and multiple sclerosis may be
48 imilar results correlating with experimental allergic encephalomyelitis and orchitis susceptibility w
49 a concomitant susceptibility to experimental allergic encephalomyelitis and significant protection ag
50 This is based on studies in experimental allergic encephalomyelitis and the demonstration that PB
51 mental models of demyelination, experimental allergic encephalomyelitis and Theiler's murine encephal
52 ls are generated in vivo during experimental allergic encephalomyelitis, and adoptively transferred T
53 ies such as multiple sclerosis, experimental allergic encephalomyelitis, and Alzheimer's disease, sug
54 inally, in the in vivo model of experimental allergic encephalomyelitis, anti-B7.2 mAb treatment abro
55 n a conventional mouse model of experimental allergic encephalomyelitis are dependent upon the produc
56 TMEV)-induced demyelination and experimental allergic encephalomyelitis are the principal immunologic
57 tolerance and developed severe experimental allergic encephalomyelitis as well as spontaneous autoim
58 st disappointing aspect of EAE [experimental allergic encephalomyelitis] as a potential model for MS
59 nical and pathological signs of experimental allergic encephalomyelitis by causing the deletion of en
60 cities in the marmoset model of experimental allergic encephalomyelitis, by means of a combinatorial
61 ity in animal models, including experimental allergic encephalomyelitis, collagen and adjuvant-induce
62 es in autoimmune destruction in experimental allergic encephalomyelitis, collagen-induced arthritis a
64 utoreactive T cell response and experimental allergic encephalomyelitis development in an IL-10-depen
65 in vivo of CD4+ T-cell-mediated experimental allergic encephalomyelitis disease in the SJL mouse mode
66 hat animals with ongoing active experimental allergic encephalomyelitis dramatically reduce the sever
67 adult male SJL are resistant to experimental allergic encephalomyelitis due to an APC-dependent induc
68 ceptibility to actively induced experimental allergic encephalomyelitis (EAE) and experimental allerg
69 l models of autoimmune disease, experimental allergic encephalomyelitis (EAE) and experimental myocar
73 two autoimmune disease models, experimental allergic encephalomyelitis (EAE) and type 1 diabetes (T1
74 igen-specific effector cells in experimental allergic encephalomyelitis (EAE) are a continuing challe
75 ment of neurological disease in experimental allergic encephalomyelitis (EAE) but not during clearanc
76 )) develop less severe clinical experimental allergic encephalomyelitis (EAE) compared to either Esr1
77 fied CTL ameliorated or blocked experimental allergic encephalomyelitis (EAE) disease mediated by MBP
79 stigation of the development of experimental allergic encephalomyelitis (EAE) in CD40L-deficient mice
83 t of fatal CD4+ T cell-mediated experimental allergic encephalomyelitis (EAE) in susceptible female L
84 sing the demyelinating model of experimental allergic encephalomyelitis (EAE) in the common marmoset.
85 udy, we used uric acid to treat experimental allergic encephalomyelitis (EAE) in the PLSJL strain of
86 5- RMTCs, prevented and treated experimental allergic encephalomyelitis (EAE) induced with MBP89-101.
89 MS is immune mediated and that experimental allergic encephalomyelitis (EAE) is a suitable model to
97 cyte glycoprotein (MOG) induced experimental allergic encephalomyelitis (EAE) is an animal model for
103 inating disease of the CNS, and experimental allergic encephalomyelitis (EAE) is its principal autoim
108 cells in multiple sclerosis and experimental allergic encephalomyelitis (EAE) lesions but their role
109 Ag-specifically treating murine experimental allergic encephalomyelitis (EAE) mediated by MBP89-101-s
111 ic autoimmune diseases, such as experimental allergic encephalomyelitis (EAE) the principal animal mo
112 tation and T cell activation in experimental allergic encephalomyelitis (EAE) was evaluated in wild-t
114 t in a second autoimmune model, experimental allergic encephalomyelitis (EAE) was induced in B10.D1-H
115 oned Th1 cells, the severity of experimental allergic encephalomyelitis (EAE) was slightly increased.
116 Gender-related differences in experimental allergic encephalomyelitis (EAE) were examined in the SJ
117 A.SW mice develop PP or SP-experimental allergic encephalomyelitis (EAE) with large areas of dem
120 sodium channels along axons in experimental allergic encephalomyelitis (EAE), a model of multiple sc
121 ent of Ag-specific Th1 cells in experimental allergic encephalomyelitis (EAE), a model of multiple sc
122 n C57BL/6 (B6) strain-dependent experimental allergic encephalomyelitis (EAE), a model of primary pro
123 gnificantly reduced severity of experimental allergic encephalomyelitis (EAE), a murine model of mult
124 lyn gene on the development of experimental allergic encephalomyelitis (EAE), a well-established Th1
125 ils a method to actively induce experimental allergic encephalomyelitis (EAE), a widely used animal m
126 ession in Lewis rats with acute experimental allergic encephalomyelitis (EAE), an animal model for MS
127 amined in Lewis rats with acute experimental allergic encephalomyelitis (EAE), an animal model for MS
128 ive cytokines and their role in experimental allergic encephalomyelitis (EAE), an animal model for mu
129 that Tkip protects mice against experimental allergic encephalomyelitis (EAE), an animal model for mu
130 been developed that ameliorate experimental allergic encephalomyelitis (EAE), an animal model for th
131 tration of UA is therapeutic in experimental allergic encephalomyelitis (EAE), an animal model of MS.
132 spinal cords of Lewis rats with experimental allergic encephalomyelitis (EAE), an animal model of MS.
133 sts reduce clinical severity of experimental allergic encephalomyelitis (EAE), an animal model of mul
134 ocess in adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of mul
136 hite matter from marmosets with experimental allergic encephalomyelitis (EAE), an animal model of mul
137 ocess of adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of rel
138 would be expected to exacerbate experimental allergic encephalomyelitis (EAE), an animal model of the
140 to multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE), but multiple additiona
141 covery from monophasic clinical experimental allergic encephalomyelitis (EAE), can be induced to deve
142 ted a model autoimmune disease, experimental allergic encephalomyelitis (EAE), even after epitope spr
143 ) of mice with actively induced experimental allergic encephalomyelitis (EAE), that expresses OX-40L.
144 d, and Ab inhibition studies in experimental allergic encephalomyelitis (EAE), the animal model for m
145 mune disease, recent studies in experimental allergic encephalomyelitis (EAE), the animal model of mu
146 autoantigen capable of inducing experimental allergic encephalomyelitis (EAE), the animal model of mu
147 mine (HA) is a key regulator of experimental allergic encephalomyelitis (EAE), the autoimmune model o
148 s and during the development of experimental allergic encephalomyelitis (EAE), the contributions of I
149 SJL/J) F(2) intercross mice to experimental allergic encephalomyelitis (EAE), the foremost animal mo
153 nd relapsing-remitting forms of experimental allergic encephalomyelitis (EAE), the principal autoimmu
154 component in susceptibility to experimental allergic encephalomyelitis (EAE), the principal autoimmu
155 , we used a murine model of MS, experimental allergic encephalomyelitis (EAE), to assess the potentia
156 stem was devised and applied to experimental allergic encephalomyelitis (EAE), to evaluate the contri
157 lycoprotein MOG(35-55)- induced experimental allergic encephalomyelitis (EAE), we assessed clinical s
158 stem for tolerance induction in experimental allergic encephalomyelitis (EAE), we created single-chai
159 tic nerves of mice induced with experimental allergic encephalomyelitis (EAE), with a focus on long-t
161 ein (MBP)-specific T cells from experimental allergic encephalomyelitis (EAE)-susceptible SJL (H-2(s)
184 s also not available for murine experimental allergic encephalomyelitis (EAE); the low number of T ce
187 ion of myelin from animals with experimental allergic encephalomyelitis had slightly lower values of
188 y resistant to the induction of experimental allergic encephalomyelitis, implying the involvement of
191 ys the onset of antigen-induced experimental allergic encephalomyelitis in myelin basic protein-T cel
194 pe switching and attenuation of experimental allergic encephalomyelitis indicate that NTB-A is import
195 usceptible to acute early-phase experimental allergic encephalomyelitis indicating that H1R signaling
196 to the amelioration of ongoing experimental allergic encephalomyelitis induced by the transfer of pr
197 aggressive T cells and reverse experimental allergic encephalomyelitis induced with free peptides.
198 ssible autoantigens, we studied experimental allergic encephalomyelitis, induced by myelin oligodendr
199 f protective cytokines prior to experimental allergic encephalomyelitis induction and decreased effec
200 and promoted protection against experimental allergic encephalomyelitis involving diverse T cell spec
202 re precisely map these TMEV and experimental allergic encephalomyelitis loci relative to each other,
203 tively reduces disease in a rat experimental allergic encephalomyelitis model of multiple sclerosis.
208 vs risk of immune deviation in experimental allergic encephalomyelitis of SJL mice induced by MP4, a
209 T cell immunity, IgG1 Abs, and experimental allergic encephalomyelitis protection, and all three wer
211 n an adoptive transfer model of experimental allergic encephalomyelitis, stimulation of lymph node ce
212 le in T cells fully complements experimental allergic encephalomyelitis susceptibility and the produc
213 R(-/-)) are more susceptible to experimental allergic encephalomyelitis than mice sufficient for the
214 ld mice are less susceptible to experimental allergic encephalomyelitis than their wild-type counterp
215 stration in a marmoset model of experimental allergic encephalomyelitis that closely resembles the hu
216 plays a key regulatory role in experimental allergic encephalomyelitis, the autoimmune model of mult
217 plays a key regulatory role in experimental allergic encephalomyelitis, the autoimmune model of mult
218 neutral proteinase (calpain) in experimental allergic encephalomyelitis, the corresponding animal mod
219 There are a variety of forms of experimental allergic encephalomyelitis, the most commonly studied an
220 n acute and relapsing-remitting experimental allergic encephalomyelitis, the neutrophil chemoattracta
221 to histamine, a subphenotype of experimental allergic encephalomyelitis, the principal autoimmune mod
223 s or CNS of wild-type mice with experimental allergic encephalomyelitis to determine their relatednes
224 se severity in animal models of experimental allergic encephalomyelitis, type I diabetes, and several
225 r histological manifestation of experimental allergic encephalomyelitis unless pertussis toxin is inj
226 e unable to resist or alleviate experimental allergic encephalomyelitis when treated with Ig-myelin o
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