ライフサイエンスコーパス: encephalitogenic

1 Paradoxically, high doses of Ag are poorly encephalitogenic.

2 g EAE, whereas other Nogo-66 epitopes can be encephalitogenic.

3 l peptide- specific T cell lines were highly encephalitogenic.

4 ing low levels of TNF-alpha) and were poorly encephalitogenic.

5 lymph node cells, compared with XY, are more encephalitogenic.

6 n suggested by some studies to be comparably encephalitogenic.

7 sion protein containing rat IFN-beta and the encephalitogenic 73-87 determinant of myelin basic prote

8 The targeting of different MOG epitopes by encephalitogenic Abs has implications for disease pathog

9 Its encephalitogenic activity has been originally linked to

10 could directly compare and characterize the encephalitogenic activity of each of these subsets upon

11 uced proliferation, IFN-gamma secretion, and encephalitogenic activity of MBP-specific T cells.

12 e recruitment of V beta 8.2+ T cells and the encephalitogenic activity of MBP73-86.

13 fter blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and periphera

14 me TCR contact residues as MOG35-55, a known encephalitogenic Ag.

15 51 (hereafter referred to as PLP1), which is encephalitogenic and induces experimental autoimmune enc

16 lls and a drastic reduction in the number of encephalitogenic and recruited inflammatory cells infilt

17 Human MOG 35-55 was only weakly encephalitogenic, and a proline substitution in rat MOG

18 sponse to rat MOG or rodent MOG 35-55, or an encephalitogenic B cell response to epitopes on human MO

19 V alpha chain sequences from two V beta8.2+-encephalitogenic, BP72-89-specific T cell clones.

20 7 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promo

21 We subsequently demonstrate that the reduced encephalitogenic capacity is due to the ability of TGF-b

22 Addition of IL-4 also reduced the encephalitogenic capacity of Th1 cultures.

23 r, and is not attributable to changes in the encephalitogenic capacity of the myelin-specific T cells

24 of MHC class II, we reported previously that encephalitogenic CD4 T cells are incapable of inducing E

25 cipient mice, suggesting direct targeting of encephalitogenic CD4 T cells.

26 ia may still play a local role in modulating encephalitogenic CD4(+) T cell responses in early EAE pr

27 susceptible animals requires reactivation of encephalitogenic CD4(+) T cells by APCs in the CNS.

28 cephalitogenic peptide to purified wild-type encephalitogenic CD4(+) T cells, indicating that CIITA-i

29 ccounts for the inhibitory effects of RTL on encephalitogenic CD4(+) T cells.

30 We show that transfer of encephalitogenic CD4(+) Th17 cells is sufficient to indu

31 iance on dendritic cells that can prime both encephalitogenic CD4Th1 and Treg cells.

32 There is no requirement for the encephalitogenic CD4Th1 cells and cytotoxic CD8Treg cell

33 A down-regulatory pathway through which encephalitogenic CD4Th1 cells are killed by CD8 regulato

34 nd the resulting CD8Treg mediated killing of encephalitogenic CD4Th1 cells.

35 Our data demonstrate that MCAM identifies encephalitogenic CD8(+) T lymphocytes, suggesting that M

36 low-level Pam2CSK4 or L654 to mice receiving encephalitogenic cells and in doing so induced both TLR2

37 nhanced disease was caused by the release of encephalitogenic cells from the periphery and the rapid

38 Encephalitogenic cells from Wt mice transferred to recip

39 KO)) recipient mice, demonstrating that once encephalitogenic cells have been generated, EAE can deve

40 Human CRP has three effects on cultured encephalitogenic cells that could contribute to the prot

41 se by directly or indirectly chemoattracting encephalitogenic cells to the CNS.

42 numbers of regulatory T cells and decreased encephalitogenic cellular infiltrates in the brain.

43 Four weeks later, mice received an encephalitogenic challenge containing guinea pig myelin

44 encephalomyelitis when administered after an encephalitogenic challenge during the onset of clinical

45 in in saline on days -21, -14, and -7 before encephalitogenic challenge on day 0 resulted in a substa

46 n) into Lewis rats either before or after an encephalitogenic challenge resulted in an attenuated cou

47 lso resistant to EAE by adoptive transfer of encephalitogenic class II-restricted CD4(+) Th1 cells, i

48 entical to those utilized by the BP-specific encephalitogenic clones described, it is likely that the

49 y cannot only inhibit systemic production of encephalitogenic cytokines by the targeted myelin oligod

50 s associated with enhanced production of the encephalitogenic cytokines TNF-alpha, IFN-gamma and IL-2

51 between lymph nodes and the CNS and produced encephalitogenic cytokines.

52 An encephalitogenic DA T cell line expressed mRNA for the T

53 y express the SJL-specific proteolipid (PLP) encephalitogenic determinant and then adoptively transfe

54 ion of autologous B cells expressing the PLP encephalitogenic determinant induced PLP-specific unresp

55 sfer of syngeneic B cells expressing the PLP encephalitogenic determinant into normal, naive, genetic

56 4, and the NAg domain comprised the dominant encephalitogenic determinant of the guinea pig myelin ba

57 n SWXJ mice primed with distinctly different encephalitogenic determinants of myelin proteolipid prot

58 rarchical order associated with the relative encephalitogenic dominance of the myelin epitopes (PLP13

59 d progression associated with their relative encephalitogenic dominance, and also persist.

60 d T cells, which suppressed proliferation of encephalitogenic DR3-restricted T cells by inducing apop

61 In this study, we show that the encephalitogenic effect of these epitopes when injected

62 hypersensitivity responses, and induction of encephalitogenic effector cells.

63 regulatory T cells (Tregs) and reduction of encephalitogenic effector T cells in the central nervous

64 d retained the ability to differentiate into encephalitogenic effectors when reactivated in vitro und

65 y high frequency of T cells responding to an encephalitogenic epitope of a myelin antigen proteolipid

66 tible SJL/J (H-2(s)) strain of mice with the encephalitogenic epitope PLP 139-151, more efficiently t

67 sponses to myelin proteolipid protein (PLP), encephalitogenic epitopes must be identified.

68 The two major encephalitogenic epitopes of PLP (PLP 139-151 and PLP 17

69 cells involved are CD4+ T cells, recognizing encephalitogenic epitopes within the central nervous sys

70 er overlapping peptides corresponding to the encephalitogenic extracellular domain of human MOG (aa 1

71 C class II domains covalently coupled to the encephalitogenic guinea pig myelin basic protein (Gp-MBP

72 in EAE induction, but whether Th17 cells are encephalitogenic has been controversial.

73 vel, it fails to expand a threshold level of encephalitogenic, high-affinity MOG-specific T cells.

74 otective effect was accompanied by a loss of encephalitogenic IFN-gamma-secreting Th cells and was re

75 eated with cefuroxime or penicillin was more encephalitogenic in adoptive transfer experiments.

76 rtion of CD8+ alphabetaTCR+ T cells that are encephalitogenic in C57BL/6 (B6) mice.

77 ice immunized with unmodified human MOG were encephalitogenic in primed B cell-deficient mice.

78 nalysis of myelin-specific T cells that were encephalitogenic in spontaneous EAE and actively induced

79 animals preimmunized and challenged with the encephalitogenic inoculum containing KLH showed either n

80 eport that lithium suppresses EAE induced by encephalitogenic interferon-gamma (IFN-gamma)-producing

81 tides, including those that are dominant and encephalitogenic, is directly related to deimination of

82 ous IL-27 potently suppressed the ability of encephalitogenic lymph node and spleen cells to transfer

83 ve transfer of either Cdk5(-/-C) or p35(-/-) encephalitogenic lymphocytes fails to transfer disease.

84 sic protein (MBP), or MBP68-86, the dominant encephalitogenic MBP epitope for this strain, administer

85 ults indicate that central tolerance to this encephalitogenic MBP epitope may not be established beca

86 Indeed, T-cell responses against the encephalitogenic MOG 91-108 epitope were greatly enhance

87 is required for presentation of the dominant encephalitogenic MOG epitope, p35-55.

88 of DR2 (DRB1*1501) covalently linked to the encephalitogenic MOG-35-55 peptide (VG312).

89 ) class II molecule covalently linked to the encephalitogenic MOG-35-55 peptide in C57BL/6 mice.

90 from EAE in Esr1-/- mice immunized with the encephalitogenic MOG-35-55 peptide was manifested phenot

91 The increased encephalitogenic MOG-restricted CD4(+) T cells were due

92 s pathogenic by decreasing the expression of encephalitogenic molecular players like GM-CSF and podop

93 ic Ab response that spreads to several other encephalitogenic myelin Ags following immunization.

94 ponses that were not cross-reactive to other encephalitogenic myelin Ags.

95 In association with the encephalitogenic myelin basic protein (MBP) 69-89 peptid

96 encephalomyelitis (EAE) when immunized with encephalitogenic myelin basic protein (MBP) peptide (MBP

97 Oral administration of encephalitogenic myelin oligodendrocyte glycoprotein (MO

98 pathogen-derived mimic of the immunodominant encephalitogenic myelin peptide PLP(139-151), which is c

99 oduction of Th1 cytokines in response to the encephalitogenic myelin peptide.

100 s who have focused T cell responses to known encephalitogenic myelin peptides.

101 lin oligodendrocyte glycoprotein (MOG) is an encephalitogenic myelin protein and a likely autoantigen

102 T cell receptor (TCR) (5B6) specific for the encephalitogenic myelin proteolipid protein (PLP) peptid

103 -mer peptide encompassing the immunodominant encephalitogenic myelin proteolipid protein (PLP139-151)

104 Mice were immunized for disease with encephalitogenic myelin proteolipid protein peptide 139

105 r heat-killed mycobacteria in the priming of encephalitogenic myelin-reactive T cells in vivo.

106 The encephalitogenic New World alphaviruses, including Venez

107 aches of attenuation can be applied to other encephalitogenic New World alphaviruses.

108 gies can be applied for attenuation of other encephalitogenic New World alphaviruses.

109 a model autoimmune disease, we delivered an encephalitogenic oligodendrocyte glycoprotein (MOG) pept

110 expressing the rearranged TCR genes from an encephalitogenic or a nonencephalitogenic PLP-139-151/I-

111 The location of myelin encephalitogenic or basic protein (BP) in peripheral ner

112 cific T cells can differentiate in vivo into encephalitogenic or regulatory T cells depending upon th

113 even after immunization with 100 micrograms encephalitogenic peptide (MBP68-86) + IFA, but were rend

114 ted the role of DC in the presentation of an encephalitogenic peptide from myelin basic protein (Ac1-

115 re appropriate presentation of the exogenous encephalitogenic peptide in association with MHC class I

116 immunization with the PLP(139-151) monomeric encephalitogenic peptide in CFA.

117 olerogenic or biasing cytokine and the major encephalitogenic peptide of guinea pig myelin basic prot

118 is capable of processing and presenting the encephalitogenic peptide of intact MOG protein.

119 ection of APCs preincubated ex vivo with the encephalitogenic peptide of myelin basic protein and eit

120 T helper cell 1 (Th1) clones specific for an encephalitogenic peptide of myelin proteolipid protein (

121 were incubated in vitro with CTLA4Ig and the encephalitogenic peptide p71-90 of myelin basic protein.

122 as compared with littermates immunized with encephalitogenic peptide plus adjuvant.

123 olipid protein (PLP)-139-151 is the dominant encephalitogenic peptide that induces experimental autoi

124 CIITA-deficient splenic APC presented encephalitogenic peptide to purified wild-type encephali

125 multaneously targeting the covalently linked encephalitogenic peptide to the MHC class II Ag processi

126 gamma and TNF-alpha) when stimulated with an encephalitogenic peptide, and induce very severe EAE upo

127 s to induce unresponsiveness in DA rats with encephalitogenic peptide-coupled splenocytes were also u

128 ive effect observed in vivo: 1) CRP inhibits encephalitogenic peptide-induced proliferation of T cell

129 ng in death occurs upon rechallenge with the encephalitogenic peptide.

130 he two principal TCR contact residues in the encephalitogenic peptide.

131 All other encephalitogenic peptides elicited, at most, a loss of t

132 l proliferative responses were seen with all encephalitogenic peptides except 142-161 and 182-201.

133 Immunocytochemistry, using gold-labeled encephalitogenic peptides of MOG and silver enhancement

134 nterferon-gamma knockout mice immunized with encephalitogenic peptides of myelin basic protein.

135 147 protected mice from EAE induced with the encephalitogenic peptides PLP-(178-191) and myelin oligo

136 lactide-co-glycolide) microparticles bearing encephalitogenic peptides prevents the onset and modifie

137 Three encephalitogenic peptides, whose autoimmune requirements

138 nd induce long-term T cell tolerance against encephalitogenic peptides.

139 coprotein (MOG) are Ig chimeras carrying the encephalitogenic PLP 139-151 and MOG 35-55 amino acid se

140 e activation of T cells stimulated with free encephalitogenic PLP peptide (PLP1), native PLP, or an I

141 sistant to disease when rechallenged with an encephalitogenic PLP peptide emulsified in CFA, indicati

142 0 specifically decreased the accumulation of encephalitogenic PLP(139-151) Ag-specific CD4+ T cells i

143 1 (Ig-PLP1) is an Ig chimera expressing the encephalitogenic PLP1 peptide corresponding to amino aci

144 The encephalitogenic potential of CD8+ MOG-specific T cells

145 odels of EAE, 3-BrPa robustly attenuates the encephalitogenic potential of EAE-driving immune cells.

146 l, cell-intrinsic factor that determines the encephalitogenic potential of inflammatory Th17 cells in

147 periments with these micro-RNAs enhanced the encephalitogenic potential of myelin-specific T cells in

148 apy induces a cytokine switch that curbs the encephalitogenic potential of PLP 139-151-specific T cel

149 Th2 cells can effectively down-regulate the encephalitogenic potential of PLP-spleen cells if presen

150 unized with hOSP(142-161) peptide, where the encephalitogenic potential of prevalent DRB1*1501/hOSP(1

151 Thus, the encephalitogenic potential of the MBP-reactive effector

152 t by immunological studies demonstrating the encephalitogenic potential of the myelin basic protein p

153 ulated, myelin-reactive T cells have greater encephalitogenic potential than resting T cells.

154 F(+) Th17 cell subset, thereby enhancing its encephalitogenic potential.

155 resulted in full-blown EAE, supporting their encephalitogenic potential.

156 rtant role in modulating the severity of the encephalitogenic process, but does not by itself contrib

157 on and/or function of cells that inhibit the encephalitogenic process.

158 Mvarphi from alpha1KO mice also enhanced the encephalitogenic property of MOG35-55-primed CD4 T cells

159 ed to examine the sequences of the two major encephalitogenic proteins of myelin, MBP and PLP, for HL

160 node T cells specific for the immunodominant encephalitogenic proteolipid protein (PLP) epitope (PLP1

161 e (HI), sharing 6 of 13 aa with the dominant encephalitogenic proteolipid protein (PLP) epitope PLP(1

162 rn mice to Ig-PLP1, a chimera expressing the encephalitogenic proteolipid protein (PLP) sequence 139-

163 an immunoglobulin (Ig) chimera carrying the encephalitogenic proteolipid protein (PLP)1 peptide corr

164 mental autoimmune encephalomyelitis using an encephalitogenic proteolipid protein peptide, PLP(139-15

165 The encephalitogenic rat T cell clone C14 recognizes the mye

166 xpand encephalitogenic T cells in vitro, the encephalitogenic repertoire is effectively outcompeted i

167 T cells escape tolerance and constitute the encephalitogenic repertoire.

168 tory T cells with suppressive effects on the encephalitogenic response.

169 elieved to be involved in the maintenance of encephalitogenic responses during the tissue damage effe

170 autoimmune encephalomyelitis due to impaired encephalitogenic responses.

171 A dose of autoantigen that is poorly encephalitogenic results in T cell hyperresponsiveness,

172 eptide in association with MHC class II, the encephalitogenic sequence was fused to a lysosomal targe

173 es spanning the murine MOBP molecule map the encephalitogenic site to amino acids 37-60.

174 owing adoptive transfer of a CD4+, Th1, VB2+ encephalitogenic SJL/J proteolipid protein peptide 139-1

175 ive transfer of EAE when cocultured with PLP-encephalitogenic spleen cells (PLP-spleen).

176 the autoreactive T cells were engaged by the encephalitogenic stimulus were able to bias their cytoki

177 he differentiation of naive CD4 T cells into encephalitogenic subsets (Th1 and Th17 cells) and concom

178 e T cells, but also in the effector phase of encephalitogenic T cell activation within the central ne

179 ecause of low Vdr gene expression and a high encephalitogenic T cell burden in the CNS.

180 y exacerbated disease symptoms and increased encephalitogenic T cell influx into the CNS.

181 a myelin oligodendrocyte glycoprotein p35-55 encephalitogenic T cell line failed to recover from the

182 Moreover, AG490 inhibits adhesion of encephalitogenic T cell lines to purified ICAM-1 and VCA

183 ific T cells, (ii) an experiment in which an encephalitogenic T cell population was successfully outc

184 resent p35-55, or an intrinsic defect in the encephalitogenic T cell repertoire, but reflects a defec

185 ILC2s remove an attenuating influence on the encephalitogenic T cell response and therefore increases

186 depending on the nature of the immunogen: an encephalitogenic T cell response to rat MOG or rodent MO

187 ogenous antigens have been found to suppress encephalitogenic T cell responses and to protect against

188 ant roles in EAE pathogenesis, by regulating encephalitogenic T cell responses, cytokine production b

189 action affects EAE development by regulating encephalitogenic T cell trafficking.

190 induce disease; however, to date, no single encephalitogenic T cell-derived cytokine has been shown

191 Although transmigration of activated encephalitogenic T cells across the blood-brain barrier

192 of these cytokines was notably decreased in encephalitogenic T cells after in vivo application of EP

193 neurons expressing YFP, we demonstrated that encephalitogenic T cells alone directed the destabilizat

194 by partially targeting the primary influx of encephalitogenic T cells and by preventing the secondary

195 to silence T-bet expression in autoreactive encephalitogenic T cells and evaluated the biological co

196 L-23 plays a critical role in development of encephalitogenic T cells and facilitates the development

197 profiles of papillomavirus peptide-specific encephalitogenic T cells and histopathology of CNS lesio

198 EAE was correlated with reduced expansion of encephalitogenic T cells and leukocyte infiltration in t

199 iosis was able to trigger the development of encephalitogenic T cells and promote the induction of EA

200 factor STAT1 in naive T cells as well as in encephalitogenic T cells and Th1 cells.

201 logues suggest that different populations of encephalitogenic T cells are activated by the C. pneumon

202 Molecules that regulate encephalitogenic T cells are of interest for multiple sc

203 inistration did not affect the activation of encephalitogenic T cells as measured by Ag-specific prol

204 ether, our results suggest that NaB modifies encephalitogenic T cells at multiple steps and that NaB

205 Our lab has demonstrated that encephalitogenic T cells can be effectively anergized by

206 1BB treatment following adoptive transfer of encephalitogenic T cells did not prevent EAE pathogenesi

207 This study provides evidence that encephalitogenic T cells directly cause reversible axona

208 ronment, could shift the cytokine profile of encephalitogenic T cells from an inflammatory Th1 to a p

209 Recipients of encephalitogenic T cells from low-dose estrogen-treated

210 In this study, we show that encephalitogenic T cells from myelin oligodendrocyte gly

211 resist EAE induced passively by transfer of encephalitogenic T cells from wild-type donors.

212 ficient mice or in immunocompetent mice with encephalitogenic T cells from wild-type Esr1+/+ or Esr1

213 Transfer of encephalitogenic T cells from wild-type mice into PD-L1(

214 ipient mice and suppressed the generation of encephalitogenic T cells in donor mice.

215 ipient mice and suppressed the generation of encephalitogenic T cells in donor mice.

216 or central nervous system (CNS) migration of encephalitogenic T cells in relapsing experimental autoi

217 cells promote the production of IFN-gamma by encephalitogenic T cells in the CNS, which is ultimately

218 NLRX1 does not alter the production of encephalitogenic T cells in the peripheral lymphatic tis

219 lated with the increase in the activation of encephalitogenic T cells in the periphery and enhanced i

220 id not impair the activation and function of encephalitogenic T cells in vitro and did not deplete in

221 de mimics effectively block the expansion of encephalitogenic T cells in vitro suggesting the potenti

222 vely APL-specific T cells are able to expand encephalitogenic T cells in vitro, the encephalitogenic

223 e CD28 peptide mimics inhibited expansion of encephalitogenic T cells in vitro.

224 ng the fate of myelin basic protein-specific encephalitogenic T cells in vivo following regulation.

225 owed an APL with the ability to expand naive encephalitogenic T cells in vivo.

226 The ability to detect the migration of encephalitogenic T cells into the central nervous system

227 pecific for CNS autoantigen and the entry of encephalitogenic T cells into the CNS during disease pro

228 ating the differentiation and persistence of encephalitogenic T cells is critical for the development

229 tingly, similar activation of CD44-deficient encephalitogenic T cells led to increased hypermethylati

230 rally immunosuppressive, neither eliminating encephalitogenic T cells nor inhibiting T cell priming.

231 i-VLA-4 either to naive recipients of primed encephalitogenic T cells or to mice 1 week after peptide

232 e T cells and to the CNS for reactivation of encephalitogenic T cells requires CCR7 and matrix metall

233 ide, a topoisomerase inhibitor, to eliminate encephalitogenic T cells significantly reduces the onset

234 he capability of activating CNS-infiltrating encephalitogenic T cells specific for immunodominant epi

235 predominant usage of Vbeta8.2 by the TCRs of encephalitogenic T cells specific for myelin basic prote

236 Thus, encephalitogenic T cells that escape tolerance either re

237 Encephalitogenic T cells that mediate experimental autoi

238 utoimmunity, we studied the ability of naive encephalitogenic T cells to expand in response to agonis

239 myelin oligodendrocyte glycoprotein-specific encephalitogenic T cells to mimic the inflammatory patho

240 ic for L-selectin had no effect on homing of encephalitogenic T cells to the brain or development of

241 Initial migration of encephalitogenic T cells to the central nervous system (

242 llenge with MOG35-55 Single-cell analysis of encephalitogenic T cells using the peptide:MHC monomer-b

243 acking gamma delta T cells, proliferation of encephalitogenic T cells was 3-fold higher, and caspase

244 In contrast, CB(2) receptor expression by encephalitogenic T cells was critical for controlling in

245 that E2-responsive, Esr1+/+ disease-inducing encephalitogenic T cells were neither necessary nor suff

246 Culture of encephalitogenic T cells with 15d-PGJ2 in the presence o

247 Furthermore, activation of CD44(+) encephalitogenic T cells with myelin oligodendrocyte gly

248 very via Fas/Fas ligand-induced apoptosis of encephalitogenic T cells, and a quick resolution of infl

249 IFN-gamma-producing cells in the CNS are the encephalitogenic T cells, and that gamma delta T cell-de

250 d GM-CSF and found that GM-CSF production by encephalitogenic T cells, but not CNS resident or other

251 ced by myelin basic protein (MBP) peptide or encephalitogenic T cells, or when EAE occurred spontaneo

252 ta suggested that signaling through CD44, in encephalitogenic T cells, plays a crucial role in the di

253 f clinical disease in adoptive recipients of encephalitogenic T cells, suggesting that CD40-CD154 int

254 We demonstrate here that encephalitogenic T cells, transduced with a retroviral g

255 However, protected rats harbor potentially encephalitogenic T cells, which are maintained in an ina

256 sion levels within the CNS demonstrated that encephalitogenic T cells, which entered a CNS environmen

257 ation and in reactivation of CNS-infiltrated encephalitogenic T cells.

258 nhances EAE development via costimulation of encephalitogenic T cells.

259 hibition required lymphocytes other than the encephalitogenic T cells.

260 less capable of generating IL-17-producing, encephalitogenic T cells.

261 sferred more severe EAE than did the control encephalitogenic T cells.

262 EAE by both priming and adoptive transfer of encephalitogenic T cells.

263 ith p35-55 or MOG or by adoptive transfer of encephalitogenic T cells.

264 peptides with potent inhibitory activity on encephalitogenic T cells.

265 severe disease due to enhanced expansion of encephalitogenic T cells.

266 ne response by myelin basic protein-reactive encephalitogenic T cells.

267 BBB, thus suppressing the transmigration of encephalitogenic T cells.

268 ut it is not required for the development of encephalitogenic T cells.

269 y precede and facilitate the infiltration of encephalitogenic T cells.

270 ty, regardless of cytokine expression by the encephalitogenic T cells.

271 lity in VWFKO mice were not due to increased encephalitogenic T-cell activity since BBB permeability

272 as a myelin basic protein-specific Tim-3(+) encephalitogenic T-cell clone (LCN-8), we found that con

273 for a T-cell receptor (TCR) derived from an encephalitogenic T-cell clone specific for the acetylate

274 of disease, but also importantly resulted in encephalitogenic T-cell infiltration and lesion formatio

275 Thus, the regulation of encephalitogenic T-cell responses and EAE susceptibility

276 ronan exacerbates CNS autoimmunity, enhances encephalitogenic T-cell responses, and suppresses the pr

277 ocytes increased the percentage of apoptotic encephalitogenic T-cells.

278 c T cells, but failed to control CNS-derived encephalitogenic T-eff that secreted interleukin (IL)-6

279 monstrate that Bhlhe40 expression identifies encephalitogenic Th cells and defines a PTX-IL-1-Bhlhe40

280 t mice develop exacerbated EAE with enhanced encephalitogenic Th1 and Th17 cell responses and reduced

281 istatin decreased the presence/activation of encephalitogenic Th1 and Th17 cells in periphery and ner

282 delayed disease onset through inhibition of encephalitogenic Th1 and Th17 immune responses.

283 d from the same precursor cell as that of an encephalitogenic Th1 cell and whether the induction was

284 This study demonstrates that an encephalitogenic Th1 cell line induces recruitment of ho

285 neously required to establish chronic EAE by encephalitogenic Th1 cells.

286 -gamma production and decreased expansion of encephalitogenic Th1 cells.

287 ction, the failure of H2RKO mice to generate encephalitogenic Th1 effector cell responses is consiste

288 TCR antagonist peptide blocks activation of encephalitogenic Th1 helper cells in vitro, but the mech

289 s essential for the generation of stable and encephalitogenic Th17 cells and for the development of E

290 endent but nonredundant roles in restraining encephalitogenic Th17 cells in vivo.

291 D25(-)CD62L(low)) that developed in vivo and encephalitogenic Th17 cells infiltrating the CNS of mice

292 at IL-1 functions as a mitogenic mediator of encephalitogenic Th17 cells rather than qualitative indu

293 -23R expression is crucial for generation of encephalitogenic Th17 cells, but its expression on the i

294 more severe disease compared with wild-type encephalitogenic Th17 cells.

295 was found to promote the differentiation of encephalitogenic Th17 cells.

296 lls and contributes to the development of an encephalitogenic Th17 population.

297 While male-derived LNCs were less encephalitogenic than female derived LNCs, cotransfer an

298 tes from male SJL mice were shown to be less encephalitogenic than MBP-specific T lymphocytes from fe

299 s, and Bhlhe40-expressing cells exhibited an encephalitogenic transcriptional signature.

300 In contrast, transfer of encephalitogenic WT cells to VIP KO hosts did not produc