ライフサイエンスコーパス: encephalitogenic

1 n suggested by some studies to be comparably encephalitogenic.

2 Paradoxically, high doses of Ag are poorly encephalitogenic.

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

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

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

6 lymph node cells, compared with XY, are more 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 e (Gpi1) selectively eliminates inflammatory encephalitogenic and colitogenic Th17 cells, without sub

16 51 (hereafter referred to as PLP1), which is encephalitogenic and induces experimental autoimmune enc

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

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

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

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

21 7 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promo

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

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

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

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

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

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

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

29 Passive transfer of these encephalitogenic CD4(+) T cells induced severe RREAE wit

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

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

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

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

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

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

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

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

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

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

40 Encephalitogenic cells from Wt mice transferred to recip

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 4, and the NAg domain comprised the dominant encephalitogenic determinant of the guinea pig myelin ba

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

59 with associated enhanced Treg frequency; and encephalitogenic, DGAT1(-/-) in vitro-polarized Th17 cel

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

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

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

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

64 hypersensitivity responses, and induction of encephalitogenic effector cells.

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

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

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

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

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

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

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

72 y IL-33-stimulated mast cells attenuated the encephalitogenic function of T cells in the experimental

73 pression of the pathogenic signature and the encephalitogenic functions of Th17 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Oral administration of encephalitogenic myelin oligodendrocyte glycoprotein (MO

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

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

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

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

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

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

107 The encephalitogenic New World alphaviruses, including Venez

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

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

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

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

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

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 as compared with littermates immunized with encephalitogenic peptide plus adjuvant.

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

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

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

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

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

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

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

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

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

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

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

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

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

135 Three encephalitogenic peptides, whose autoimmune requirements

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

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

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

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

140 1 (Ig-PLP1) is an Ig chimera expressing the encephalitogenic PLP1 peptide corresponding to amino aci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 The encephalitogenic rat T cell clone C14 recognizes the mye

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

164 T cells escape tolerance and constitute the encephalitogenic repertoire.

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

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

167 autoimmune encephalomyelitis due to impaired encephalitogenic responses.

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

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

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

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

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

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

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

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

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

177 ng functions and were ineffective in driving encephalitogenic T cell differentiation.

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

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

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

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

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

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

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

185 y tryptophan restriction results in impaired encephalitogenic T cell responses and is accompanied by

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

187 microbiota, which in turn have an impact on encephalitogenic T cell responses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 ults presented from the adoptive transfer of encephalitogenic T cells between wild-type and GADD34 mu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 Thus, encephalitogenic T cells that escape tolerance either re

235 Encephalitogenic T cells that mediate experimental autoi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 nhances EAE development via costimulation of encephalitogenic T cells.

258 hibition required lymphocytes other than the encephalitogenic T cells.

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

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

261 ut it is not required for the development of 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 BBB, thus suppressing the transmigration of encephalitogenic T cells.

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

268 Moreover, encephalitogenic T lymphocytes from IFN-alpha-treated mi

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

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

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

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

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

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

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

276 particularly suited to control corresponding encephalitogenic Tcon responses and likely contribute to

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

278 ignature and pathogenic memory of a discrete encephalitogenic Th subset.

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

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

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

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

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

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

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

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

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

288 promotes the pathogenic effector program of encephalitogenic Th17 cells by regulating GM-CSF via Bhl

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

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

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

292 -23R expression is crucial for generation of encephalitogenic Th17 cells, but its expression on the i

293 with Staphylococcus aureus and, by licensing encephalitogenic Th17 cells, played a key role in the de

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

295 more severe disease compared with wild-type 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