ライフサイエンスコーパス: alpha-GalCer

1 alpha-GalCer administration in EAMG mice increased the s

2 alpha-GalCer injection also induced a marked increase in

3 alpha-GalCer was administered by the intranasal route be

4 alpha-GalCer was unable to protect IL-4 KO and IL-10 KO

5 alpha-GalCer-induced liver injury was significantly supp

6 overy in 1995 of alpha-galactosylceramide 1 (alpha-GalCer), also known as KRN7000,1 hundreds of compo

7 screening assays on a focused library of 25 alpha-GalCer analogues.

8 In addition, alpha-GalCer treatment of the IFN-gamma(-/-) mice exacer

9 of IRF-1 by RNA interference did not affect alpha-GalCer-induced NKT cell activation.

10 ls increase their cytotoxic properties after alpha-GalCer injection, resulting in an increase in kill

11 hich is attributable to iNKT tolerance after alpha-GalCer injection.

12 hibition of BTLA by anti-BTLA mAb aggravates alpha-GalCer-induced hepatic injury in CD160(-/-) mice,

13 Although alpha-GalCer-transactivated pre-mNK cells lost their cap

14 Its activity was also investigated in an alpha-GalCer-induced murine models, including lung infla

15 isingly, one of the novel carbamate analogs, alpha-GalCer-6''-(pyridin-4-yl)carbamate, formed novel i

16 nisolone administration attenuated ConA- and alpha-GalCer-induced hepatitis and systemic inflammatory

17 the rate of dissociation of alpha-GalCer and alpha-GalCer analogues from hCD1d molecules.

18 N1 A/California/04/2009 (kCA04) SI virus and alpha-GalCer induced high titers of anti-hemagglutinin a

19 ge proportion of Valpha24(+)CD3(+) cells are alpha-GalCer-CD1d-Tet(+)CD3(+) iNKT cells, which primari

20 As alpha-GalCer stimulates both human and murine NKT cells,

21 binds to CD1d with the same conformation as alpha-GalCer.

22 The TCR binds to HS44 similarly as alpha-GalCer, but forms less contacts, thus explaining i

23 could block the loading of lipid Ags such as alpha-GalCer, and consequently inhibited NKT recognition

24 lian alpha-linked glycosylceramides, such as alpha-GalCer.

25 Because alpha-GalCer is a marine-sponge-derived ligand, our stud

26 Because alpha-GalCer recognition by NKT cells is conserved among

27 However, both alpha-GalCer-dependent and cytokine-dependent activation

28 Upon activation by alpha-GalCer, invariant NKT cells secrete multiple cytok

29 , whereas strong activation of iNKT cells by alpha-GalCer accelerates CCl(4)-induced acute liver inju

30 Activation of iNKT cells by alpha-GalCer induces the production of IFN-gamma, which

31 Protection of disease conferred by alpha-GalCer correlated with its ability to suppress mye

32 ctivation of NK T cells in CD1d(+/+) mice by alpha-GalCer resulted in reduced illness and delayed vir

33 ed suppressor cells (MDSCs) in the spleen by alpha-GalCer that might attenuate its antitumor efficacy

34 mouse liver was dramatically upregulated by alpha-GalCer treatment.

35 alpha-galactosylceramide presented by CD1d (alpha-GalCer/CD1d).

36 with CD1d-4',4''-deoxy-alpha-GalCer and CD1d-alpha-GalCer with a shorter, di-unsaturated acyl chain (

37 The frequency of CD1d-alpha-GalCer-restricted NKT cells in the liver was also

38 ng strategies and specificities towards CD1d-alpha-GalCer and related antigens, thus providing far gr

39 umbers Sand functions of NKT (TCRbeta(+)CD1d/alpha-GalCer tetramer(+)) cells, particularly of the NK1

40 cells failed to directly recognize the CD1d/alpha-GalCer complex.

41 of the TCR-beta chain on the avidity of CD1d:alpha-GalCer binding.

42 cytes loaded with alpha-galactosyl ceramide (alpha-GalCer) could stimulate IFN-gamma production and C

43 to the glycolipid alpha-galactosyl ceramide (alpha-GalCer) presented by CD1d, and they may have impor

44 lycolipid antigen alpha-galactosyl ceramide (alpha-GalCer) were dampened by prior autoreactive activa

45 NKT cell agonist alpha-galactosyl ceramide (alpha-GalCer), bacterial glycolipids, and variations of

46 NKT cell ligand, alpha-galactosyl-ceramide (alpha-GalCer; KRN-7000) in five patients who had advance

47 mCD1d is similar to that of the short-chain alpha-GalCer ligand PBS-25, but its sphinganine chain is

48 Finally, chronic alpha-GalCer treatment had little effect on liver injury

49 show that targeting nanoparticles containing alpha-GalCer and Ag to CD8alpha(+) DCs promotes potent a

50 In contrast, alpha-GalCer, a synthetic homologue of microbial alpha-g

51 moiety or other substitutions that decrease alpha-GalCer flexibility would stabilize the F'-pocket.

52 an NKT TCR in complex with CD1d-4',4''-deoxy-alpha-GalCer and CD1d-alpha-GalCer with a shorter, di-un

53 of Valpha14i NKT cells clearly discriminated alpha-GalCer bound to mouse or human CD1d on the basis o

54 Gb3 and, in the other, a smaller cavity fits alpha-GalCer more snugly.

55 significantly reduced liver injury following alpha-GalCer treatment.

56 ion of MDSC via IL-33 as a new mechanism for alpha-GalCer-elicited immunosuppression but also provide

57 yte-derived IRF-1 was mainly responsible for alpha-GalCer-induced liver injury, based on the observat

58 Nevertheless, DCs from mice given free alpha GalCer are able to induce strong IFN-gamma-produci

59 an recognize cellular antigens distinct from alpha-GalCer and identify phospholipids as potential sel

60 conversely, adoptive transfer of MDSCs from alpha-GalCer-treated mice ameliorated passive EAE induce

61 Furthermore, alpha-GalCer promoted NKT cells to transcribe the IL-2 g

62 Furthermore, alpha-GalCer was unable to protect CD1d knockout (KO) mi

63 Furthermore, alpha-GalCer-induced egr-2/3 in hepatic NKT cells upregu

64 lycolipid antigen, alpha-galactosylceramide (alpha GalCer), to the mouse NK-T cell hybridoma, DN32.D3

65 he glycolipid drug alpha-galactosylceramide (alpha GalCer), which triggers release of large amounts o

66 lipid Ags such as alpha-galactosylceramide (alpha GalCer).

67 derived glycolipid alpha-galactosylceramide (alpha GalCer).

68 glycosphingolipid alpha-galactosylceramide (alpha-GalCer(Bf)), which is structurally related to a sp

69 of iNKT activator alpha-galactosylceramide (alpha-GalCer) accelerates CCl(4)-induced acute liver inj

70 ith use of mucosal alpha-galactosylceramide (alpha-GalCer) administration, is a promising approach to

71 repertoire and how alpha-galactosylceramide (alpha-GalCer) analogues induce distinct functional respo

72 ha 14 NKT cells by alpha-galactosylceramide (alpha-GalCer) and CD1d potentiates Th2-mediated adaptive

73 colipid ligands of alpha-galactosylceramide (alpha-GalCer) and have determined the structures of a hu

74 ith the glycolipid alpha-galactosylceramide (alpha-GalCer) and myelin-reactive T cells potentiates EA

75 ein complexed with alpha-galactosylceramide (alpha-GalCer) and quantitated hCD1d tetramer reactive ce

76 ion in response to alpha-galactosylceramide (alpha-GalCer) and reduced iNKT cell-mediated lysis of wi

77 ith the glycolipid alpha-galactosylceramide (alpha-GalCer) are a distinct lymphocyte sublineage.

78 ramers loaded with alpha-galactosylceramide (alpha-GalCer) bind selectively to mouse invariant Valpha

79 synthetic antigen alpha-galactosylceramide (alpha-GalCer) binds CD1d.

80 lycolipids such as alpha-galactosylceramide (alpha-GalCer) by the NKT cell TCR (NKTCR) obeys a key-lo

81 y the superagonist alpha-galactosylceramide (alpha-GalCer) can protect against cancer, autoimmune dis

82 of NKT cells with alpha-galactosylceramide (alpha-GalCer) causes liver injury through mechanisms tha

83 The glycolipid alpha-galactosylceramide (alpha-GalCer) has been shown to bind CD1d molecules to a

84 y to fight cancer, alpha-galactosylceramide (alpha-GalCer) has been used to activate NKT cells.

85 (iNKT) cell ligand alpha-galactosylceramide (alpha-GalCer) holds great promise in cancer therapy, alt

86 Administration of alpha-galactosylceramide (alpha-GalCer) in animals enhances antitumor immunity via

87 to the NKT ligand alpha-galactosylceramide (alpha-GalCer) in both healthy donors and patients with m

88 administration of alpha-galactosylceramide (alpha-GalCer) induced late PTB and neonatal mortality.

89 nthetic glycolipid alpha-galactosylceramide (alpha-GalCer) induces long-term NKT cell unresponsivenes

90 cell activation by alpha-galactosylceramide (alpha-GalCer) inhibits autoimmune diabetes in NOD mice,

91 h the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the development of T-cell-mediate

92 administration of alpha-galactosylceramide (alpha-GalCer) intranasally.

93 The glycolipid alpha-galactosylceramide (alpha-GalCer) is a potent and specific activator of mous

94 alpha-Galactosylceramide (alpha-GalCer) is a potent NKT cell agonist when presente

95 alpha-Galactosylceramide (alpha-GalCer) is an iNKT cell-specific glycolipid Ag: a

96 alpha-Galactosylceramide (alpha-GalCer) is the prototypic agonist, but its excessi

97 glycolipid ligand alpha-galactosylceramide (alpha-GalCer) or the sphingosine-truncated alpha-GalCer

98 olipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the MHC class I-like molecule

99 glycosphingolipid alpha-galactosylceramide (alpha-GalCer) protects susceptible mice against EAE.

100 ysical analyses of alpha-galactosylceramide (alpha-GalCer) recognition by a human CD1d-restricted TCR

101 alpha-Galactosylceramide (alpha-GalCer) represents a new class of immune stimulato

102 ith the glycolipid alpha-galactosylceramide (alpha-GalCer) results in the acquisition of a hyporespon

103 glycolipid ligand alpha-galactosylceramide (alpha-GalCer) stimulate a wide array of immune responses

104 cine incorporating alpha-galactosylceramide (alpha-GalCer) that targets the immune adjuvant propertie

105 agonist glycolipid alpha-galactosylceramide (alpha-GalCer) to a fetal thymic organ culture (FTOC) ind

106 alpha-Galactosylceramide (alpha-GalCer), a specific ligand for iNKT cells, was use

107 of vorinostat with alpha-galactosylceramide (alpha-GalCer), an IFN-gamma-inducing agent, was signific

108 valin A (ConA) and alpha-galactosylceramide (alpha-GalCer), and hepatotoxin-mediated hepatitis induce

109 quires the agonist alpha-galactosylceramide (alpha-GalCer), as opposed to the nonantigenic beta-galac

110 glycolipid ligand, alpha-galactosylceramide (alpha-GalCer), causes bystander activation of NK, B, CD4

111 KT cell antigen is alpha-galactosylceramide (alpha-GalCer), derived from the marine sponge.

112 nist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the development of EAMG.

113 al NKT cell ligand alpha-galactosylceramide (alpha-GalCer), originally isolated from a marine sponge,

114 ge-derived reagent alpha-galactosylceramide (alpha-GalCer), results in the rapid production of a vari

115 cantly weaker than alpha-galactosylceramide (alpha-GalCer), the most potent known NKT agonist.

116 cell superagonist, alpha-galactosylceramide (alpha-GalCer), which stimulates a wide array of anti-vir

117 ibody specific for alpha-galactosylceramide (alpha-GalCer)-human CD1d (hCD1d) complexes, we measured

118 s, OVA-induced and alpha-galactosylceramide (alpha-GalCer)-induced AHR.

119 n of GD3 inhibited alpha-galactosylceramide (alpha-GalCer)-induced NKT cell activation in a dose-depe

120 es generated using alpha-galactosylceramide (alpha-GalCer)-loaded CD1d tetramers.

121 o human NKT cells, alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells activate and expand

122 lls activated with alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells were profoundly mor

123 population of CD1d-alpha-galactosylceramide (alpha-GalCer)-reactive human NKT cells that differ marke

124 -gamma and IL-4 by alpha-galactosylceramide (alpha-GalCer)-stimulated liver NKT cells in a PGE2 E-typ

125 s ligands, such as alpha-galactosylceramide (alpha-GalCer).

126 th the NKT ligand, alpha-galactosylceramide (alpha-GalCer).

127 estricted antigen, alpha-galactosylceramide (alpha-GalCer).

128 (NKT)-cell agonist alpha-galactosylceramide (alpha-GalCer).

129 ivo challenge with alpha-galactosylceramide (alpha-GalCer).

130 olipid Ags such as alpha-galactosylceramide (alpha-GalCer).

131 ed iNKT cells with alpha-galactosylceramide (alpha-GalCer).

132 binding glycolipid alpha-galactosylceramide (alpha-GalCer).

133 T cells recognized alpha-galactosylceramide (alpha-GalCer); however, their fine specificity for other

134 uman CD1d-tetramer loaded with alpha-GalCer (alpha-GalCer-CD1d-Tet), we found that alpha-GalCer-CD1d-

135 Glycolipid alpha-GalCer treatment of mice induced the expression of

136 ing exogenous NKT cell activator, glycolipid alpha-GalCer, and endogenous prostaglandin E2 (PGE2).

137 doped with alpha-hydroxygalactosylceramide (alpha-GalCer) was very similar to that observed with Gal

138 , necessary but not sufficient for imparting alpha-GalCer/CD1d recognition.

139 Importantly, alpha GalCer-activated NKT cells restricted the growth o

140 Importantly, alpha-GalCer was used to induce CD8(+) T cells to antige

141 dendritic cells (DC) play a critical role in alpha GalCer-mediated activation of iNKT cells and subse

142 cient iNKT cells display profound defects in alpha-GalCer-induced activation and cytokine production.

143 to characterize the key pathways involved in alpha-GalCer-induced liver injury.

144 n of either TNF-alpha or IFN-gamma inhibited alpha-GalCer-mediated IRF-1 upregulation.

145 only in piglets that had received intranasal alpha-GalCer.

146 ingle therapeutic vaccination of irradiated, alpha-GalCer-loaded autologous tumor cells was sufficien

147 cells did not stain for DX5 or with labeled alpha-GalCer CD1d tetramer, suggesting an absence of NK

148 on by iNKT cells, in contrast to the ligands alpha-GalCer (both IFN-gamma and IL-4) and OCH (primaril

149 Nevertheless, alpha GalCer presentation by B cells elicits low IL-4 re

150 In this study, we describe novel alpha-GalCer-loaded mouse and human CD1d-IgG1 dimers, wh

151 While developing novel alpha-GalCer analogs that were meant to be utilized as p

152 lso after treatment of neonatal mice with Nu-alpha-GalCer, which effectively increased DN CD38(hi) NK

153 berculosis, we asked whether the addition of alpha GalCer could be used to induce effector functions

154 Presentation of alpha GalCer by CD1d-transfected T84 cells (T84d) to DN3

155 he induction of anergy after presentation of alpha GalCer on other cells.

156 We also tested the ability of alpha-GalCer as an adjuvant to modulate the type 2 immun

157 Finally, the ability of alpha-GalCer to reduce the pulmonary metastatic burden o

158 se prevention correlated with the ability of alpha-GalCer to suppress interferon-gamma but not interl

159 alterations in the therapeutic activities of alpha-GalCer.

160 The adjuvant activity of alpha-GalCer enhances both priming and boosting of CD8(+

161 Administration of alpha-GalCer also upregulated the expression of inflamma

162 olleagues demonstrate that administration of alpha-GalCer causes iNKT cells to become unresponsive, f

163 Unfortunately, administration of alpha-GalCer causes long-term NKT cell anergy, but the m

164 , we show that concomitant administration of alpha-GalCer delayed B. anthracis systemic dissemination

165 Yet, administration of alpha-GalCer in the second trimester did not cause pregn

166 Administration of alpha-GalCer in the third trimester induced an increase

167 Administration of alpha-GalCer in the third trimester suppressed PPARgamma

168 to ask, should sequential administration of alpha-GalCer still be used to activate iNKT cells given

169 In vivo administration of alpha-GalCer to mice results in the rapid activation of

170 ntranasal but not systemic administration of alpha-GalCer to piglets infected with pandemic A/Califor

171 urprisingly, we found that administration of alpha-GalCer, which very specifically activates iNKT cel

172 In contrast, analogs of alpha-GalCer containing phenyl group in the lipid tail c

173 lysis of a series of novel 6''-OH analogs of alpha-GalCer with more potent antitumor characteristics.

174 ocessing of a lysosome-dependent analogue of alpha-GalCer was impaired in all the strains of mice tes

175 of mice to a set of structural analogues of alpha-GalCer.

176 ould have reflected the unique attributes of alpha-GalCer, using several related glycolipid compounds

177 Our study shows that coadministration of alpha-GalCer with suboptimal doses of irradiated sporozo

178 We also show that coadministration of alpha-GalCer with various different immunogens strongly

179 We report that codelivery of alpha-GalCer and protein Ag to CD8alpha(+) DCs triggers

180 Furthermore, targeted delivery of alpha-GalCer to CD8alpha(+) DCs, by means of anti-DEC205

181 ues and assessed the rate of dissociation of alpha-GalCer and alpha-GalCer analogues from hCD1d molec

182 n this report, we show that a single dose of alpha-GalCer before T. cruzi infection decreases parasit

183 current study, we investigated the effect of alpha-GalCer against Bacillus anthracis infection, the a

184 on of IL-2 reduced the therapeutic effect of alpha-GalCer in this model.

185 dLNs) and prevented the protective effect of alpha-GalCer on bacterial dissemination out of the dLNs.

186 artially eliminated the inhibitory effect of alpha-GalCer on liver regeneration.

187 The modulatory effect of alpha-GalCer requires the CD1d antigen presentation path

188 of MDSCs abrogated the protective effects of alpha-GalCer against EAE and, conversely, adoptive trans

189 Here, we review the effects of alpha-GalCer in (pre)clinics and discuss current and fut

190 h in turn mediate the therapeutic effects of alpha-GalCer in EAMG.

191 In these different models, the effects of alpha-GalCer mainly relied on the establishment of a typ

192 The adjuvant effects of alpha-GalCer require CD1d molecules, Valpha14 NKT cells,

193 cell response and abolishes the efficacy of alpha-GalCer as an adjuvant for antitumor vaccines.

194 e CD1 surface compared with the galactose of alpha-GalCer.

195 Injection of alpha-GalCer before or after PHx, which rapidly stimulat

196 Injection of alpha-GalCer-pulsed, but not unpulsed, dendritic cells (

197 However, repeated injections of alpha-GalCer result in long-term unresponsiveness or ane

198 CR to hCD1d molecules loaded with a panel of alpha-GalCer analogues and assessed the rate of dissocia

199 nd iNKT cell activation by the same panel of alpha-GalCer analogues.

200 tly, more AI4 T cells accumulated in PLNs of alpha-GalCer than PBS-treated recipients, while no diffe

201 al accumulation of mature DCs in the PLNs of alpha-GalCer-treated NOD mice, followed by a substantial

202 ion in comparison with the 3'-OH position of alpha-GalCer, which contrasts the fine specificity of th

203 cell targeting, we show that presentation of alpha-GalCer by DCs not only triggers optimal primary iN

204 the stimulatory and regulatory properties of alpha-GalCer derivatives.

205 rosiglitazone treatment, reduced the rate of alpha-GalCer-induced late PTB and improved neonatal surv

206 Because recognition of alpha-GalCer by NKT cells is phylogenetically conserved,

207 3alpha loop is sufficient for recognition of alpha-GalCer despite CDR1alpha and CDR2alpha sequence va

208 Furthermore, a multiple dose regimen of alpha-GalCer before T. cruzi infection does not lower pa

209 One alpha-GalCer-reactive, Valpha24-positive clone differed

210 ies) and were required to achieve an optimal alpha-GalCer-induced immune response.

211 madelta T cells were required for an optimal alpha-GalCer-mediated anti-tumor activity.

212 However, immunized CD1-deficient or alpha-GalCer-treated wild-type mice did not exhibit dimi

213 neous AHR as well as AHR induced with OVA or alpha-GalCer were all eliminated by blocking CD1d, the r

214 ited the IL-17A production by poly(I:C) plus alpha-GalCer in the same models.

215 overexpression of IRF-1 greatly potentiated alpha-GalCer-induced liver injury.

216 The MODE-K cell line could also present alpha GalCer to primary mouse NK-T cells.

217 The human IEC line, T84, mainly presented alpha GalCer when transfected with human CD1d.

218 of Jalpha18-positive TCRs that can recognize alpha-GalCer.

219 cell deficiency can be corrected by repeated alpha-GalCer treatment and that NKT cells may play a pro

220 Replacing alpha-GalCer with beta-mannosylceramide resulted in prol

221 r into an orientation that closely resembles alpha-GalCer.

222 ta sequences in some anti-peptide responses, alpha-GalCer-reactive T cells have polyclonal CDR3beta s

223 ly related to a sponge-derived sphingolipid (alpha-GalCer, KRN7000) that is the prototypical agonist

224 induced NKT anergy in response to subsequent alpha-GalCer stimulation.

225 hat exhibits a superior adjuvant effect than alpha-GalCer on HIV and malaria vaccines in mice.

226 We hypothesized that alpha GalCer presentation by different CD1d-positive cel

227 We demonstrate that alpha-GalCer(Bf) has similar immunological properties to

228 alCer (alpha-GalCer-CD1d-Tet), we found that alpha-GalCer-CD1d-Tet(+) CD3(+) iNKT cells make up 0.13%

229 ice and humans, these findings indicate that alpha-GalCer might be useful for therapeutic interventio

230 We show that alpha-GalCer induced the expansion and immunosuppressive

231 Here we show that alpha-GalCer prevents development of diabetes in wild-ty

232 In this study, we showed that alpha-GalCer-triggered egr2/3, which induced programmed

233 cription (STAT)1 significantly abolished the alpha-GalCer-mediated inhibition of liver regeneration.

234 reactive Valpha14+ T cell line conferred the alpha-GalCer/CD1d specificity without induction of autor

235 the role of TCRbeta chain in determining the alpha-GalCer/CD1d vs autoreactive specificity of Valpha1

236 n receptor (TCR) has a high affinity for the alpha-GalCer/CD1d complex, driven by a long half-life (t

237 ed for IL-12 and IL-18 has been shown in the alpha-GalCer-induced IFN-gamma production by gammadelta

238 e show that DPPE-PEG completely inhibits the alpha-GalCer-induced phosphorylation of ERK tyrosine kin

239 Phenyl ring substitutions of the alpha-GalCer fatty acid moiety were recently found to be

240 In mice lacking germline Vbeta8, most of the alpha-GalCer-reactive T cells express either Vbeta2 or V

241 nd, at 1.6-1.9 A resolution, reveal that the alpha-GalCer phenyl analogues impart minor structural di

242 as a relatively high-affinity binding to the alpha-GalCer/CD1d complex, with a particularly slow off

243 Therefore, alpha-GalCer treatment might be used to increase protect

244 Therefore, alpha-GalCer treatment skewed pre-mNK cell responses awa

245 Thus, alpha-GalCer-activated NKT cells can induce expansion of

246 Thus, alpha-GalCer-induced FasL/TRAIL and IL-33 provided a nov

247 d, and exerted lytic activity in response to alpha GalCer-pulsed monocyte-derived cells.

248 d to naive mice, but not when transferred to alpha GalCer-treated recipients.

249 oenvironment that induced NKT cell anergy to alpha-GalCer restimulation.

250 onstrate that DPPE-PEG acts as antagonist to alpha-GalCer and competes with alpha-GalCer for binding

251 er studies revealed that IL-4 contributed to alpha-GalCer-induced iNKT cell expansion and IFN-gamma p

252 study to characterize mechanisms leading to alpha-GalCer-mediated protection against lethal infectio

253 that are CD1d restricted but nonreactive to alpha-GalCer are activated in response to hepatocytes ex

254 hich are CD1d-restricted, but nonreactive to alpha-GalCer.

255 TSC1 in iNKT cells results in resistance to alpha-GalCer-induced anergy, manifested by increased exp

256 e like T lymphocytes that rapidly respond to alpha-GalCer presented by CD1d via the production of bot

257 sion, and induction of anergy in response to alpha-GalCer administration resemble the responses of co

258 nd may be related to the intense response to alpha-GalCer by NKT cells in vivo.

259 ut the dynamics of the iNKT cell response to alpha-GalCer in vivo.

260 iNKT cells produce IFN-gamma in response to alpha-GalCer, as shown by ELISpot assay and intracellula

261 amplify the innate and acquired response to alpha-GalCer, with possibly important outcomes for the t

262 c for cytomegalovirus in vivo in response to alpha-GalCer-loaded DCs, but not unpulsed DCs.

263 d hepatocytes expressed IRF-1 in response to alpha-GalCer.

264 e investigating mouse iNKT cell responses to alpha-GalCer in vivo, we found a dramatically enlarged t

265 wittichii, although structurally similar to alpha-GalCer, have significant differences in the sugar

266 pha24-negative clones responded similarly to alpha-GalCer and a closely related bacterial analog, sug

267 s and produce an adjuvant effect superior to alpha-GalCer, we performed step-wise screening assays on

268 Their sensitivity towards alpha-GalCer was comparable to a murine iNKT hybridoma c

269 However, in phase I clinical trials, alpha-GalCer was shown to display only marginal biologic

270 (alpha-GalCer) or the sphingosine-truncated alpha-GalCer analog OCH leads to CD40 signaling as well

271 IL-33 provided a novel mechanism underlying alpha-GalCer-induced hepatotoxicity and MDSC accumulatio

272 vealed that fetuses from mice that underwent alpha-GalCer-induced late PTB had bradycardia and died s

273 ed to proliferate and produce IFN-gamma upon alpha-GalCer restimulation but retained the capacity to

274 characteristic cytokine storm produced upon alpha-GalCer activation was not induced.

275 in the design of treatment regimens that use alpha-GalCer as a specific activator of iNKT cells.

276 When alpha GalCer is administered to mice on dendritic cells

277 Therefore, when alpha GalCer is selectively targeted to DCs, mice develo

278 ed the migration of IDENs to the liver where alpha-GalCer and PGE2 induced NKT anergy in response to

279 In the current study, we evaluated whether alpha-GalCer generates protective immunity against a swi

280 e unresponsive to subsequent activation with alpha-GalCer.

281 nd that activation of anergic NKT cells with alpha-GalCer exacerbated, rather than prevented, B16 met

282 dition, direct activation of iNKT cells with alpha-GalCer, which induced AHR in wild-type mice, faile

283 the sulfatides in a fashion comparable with alpha-GalCer.

284 HS44 is a weaker agonist compared with alpha-GalCer in vitro, although in vivo it induces robus

285 ency of the microbial antigens compared with alpha-GalCer.

286 l-based stimulatory activities compared with alpha-GalCer.

287 antagonist to alpha-GalCer and competes with alpha-GalCer for binding to CD1d.

288 ic glycolipid Ag: a single immunization with alpha-GalCer stimulates robust IFN-gamma and IL-4 produc

289 Moreover, the interactions with alpha-GalCer differ between the type I and these atypica

290 rst, using a human CD1d-tetramer loaded with alpha-GalCer (alpha-GalCer-CD1d-Tet), we found that alph

291 iated lysis of wild-type targets loaded with alpha-GalCer.

292 ding to CD1d-Fc fusion tetramers loaded with alpha-GalCer.

293 ted that immunization of wild-type mice with alpha-GalCer enhanced the adaptive immune response elici

294 recipients, but not in those pretreated with alpha-GalCer (8%).

295 ating MDSCs in mice injected repeatedly with alpha-GalCer were 2-fold higher than those treated with

296 Upon restimulation with alpha-GalCer-pulsed CD1d(+) cells, macaque NKT cells sec

297 After stimulation with alpha-GalCer, an antigen recognized by NKT cells, these

298 onger responsive to further stimulation with alpha-GalCer-loaded CD1d-expressing cells.

299 Repeated treatments with alpha-GalCer result in the expansion of NKT cells and al

300 Vaccination with alpha-GalCer resulted in a systemic increase in NKT-cell