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1 ed T cells cross-reacting against CD1d-alpha-galactosylceramide.
2 h glycolipid Ags, such as the model Ag alpha-galactosylceramide.
3 on than the invariant NKT cell agonist alpha-galactosylceramide.
4 ty than the most potent agonist known, alpha-galactosylceramide.
5 n almost identical fatty acyl chain as alpha-galactosylceramide.
6 sing the invariant NKT-specific ligand alpha-galactosylceramide.
7 ctivation of Valpha14 iNKT cells using alpha-galactosylceramide.
8 unique GSLs structurally derived from alpha-galactosylceramide.
9 ivo and in vitro after activation with alpha-galactosylceramide.
10 stimulatory invariant NKT cell agonist alpha-galactosylceramide.
11 1d-dependent manner in the presence of alpha-galactosylceramide.
12 ferative defect after stimulation with alpha-galactosylceramide.
13 in intact lymphoid tissues, we studied alpha-galactosylceramide.
14 on of natural killer T cells by ligand alpha-galactosylceramide.
15 o achieve high affinity recognition of alpha-galactosylceramide.
16 rations after NKT cell activation with alpha-galactosylceramide.
17 following activation with CD1d ligand alpha-galactosylceramide.
18 e II NKT cells, which do not recognize alpha-galactosylceramide.
19 vision of a defined exogenous antigen, alpha-galactosylceramide.
20 t needing the iNKT cell agonist ligand alpha-galactosylceramide.
21 ponsive to activation with the antigen alpha-galactosylceramide.
23 the rate of transfer of anthrylvinyl-labeled galactosylceramide (1 mol %) from a donor to acceptor ve
24 lar vesicles composed of 1 mol% anthrylvinyl-galactosylceramide, 1.5 mol% perylenoyl-triglyceride, an
25 ree novel subspecies of sphingolipids, alpha-galactosylceramides, 4,5-dihydroceramides, and 1-deoxysp
26 of the transbilayer distribution of [6-(13)C]galactosylceramide (99.8% isotopic enrichment) was achie
27 The fyn(-/-) NK T cells respond to alpha-galactosylceramide, a ligand recognized by NK T cells, a
30 In addition, injection of mice with alpha-galactosylceramide, a specific glycolipid agonist of iNK
32 Corollarily, treatment of mice with alpha-galactosylceramide--a lipid that activates CD1d-restrict
33 ion from the saposin B deficiency diminished galactosylceramide accumulation in the brain and kidney
34 that the downstream effects induced by alpha-galactosylceramide activated NK T cells on NK cells are
36 -gamma and IL-4 production, while oral alpha-galactosylceramide activated NKT2 cells in the mesenteri
38 he addition of either TiterMax Gold or alpha-galactosylceramide adjuvant, though adjuvant reduced cel
40 icrobial immune response suggests that alpha-galactosylceramide administration could have a role in n
41 esence or absence of iNKT-cell agonist alpha-galactosylceramide, after which OTI T-cell priming, anti
42 of the functional glycolipid antigen, alpha-galactosylceramide (alpha GalCer), to the mouse NK-T cel
43 rapid reaction to the glycolipid drug alpha-galactosylceramide (alpha GalCer), which triggers releas
47 ird compound was the glycosphingolipid alpha-galactosylceramide (alpha-GalCer(Bf)), which is structur
48 KT through injection of iNKT activator alpha-galactosylceramide (alpha-GalCer) accelerates CCl(4)-ind
49 eta T lymphocytes, with use of mucosal alpha-galactosylceramide (alpha-GalCer) administration, is a p
50 receptor beta-chain repertoire and how alpha-galactosylceramide (alpha-GalCer) analogues induce disti
51 activation of V alpha 14 NKT cells by alpha-galactosylceramide (alpha-GalCer) and CD1d potentiates T
52 reduces CD1d-mediated presentation of alpha-galactosylceramide (alpha-galcer) and endogenous antigen
53 against altered glycolipid ligands of alpha-galactosylceramide (alpha-GalCer) and have determined th
54 tion of NK T cells with the glycolipid alpha-galactosylceramide (alpha-GalCer) and myelin-reactive T
55 ecombinant CD1d protein complexed with alpha-galactosylceramide (alpha-GalCer) and quantitated hCD1d
56 of cytokine production in response to alpha-galactosylceramide (alpha-GalCer) and reduced iNKT cell-
57 ) T cells reactive with the glycolipid alpha-galactosylceramide (alpha-GalCer) are a distinct lymphoc
60 hat recognition of glycolipids such as alpha-galactosylceramide (alpha-GalCer) by the NKT cell TCR (N
61 t NKT (iNKT) cells by the superagonist alpha-galactosylceramide (alpha-GalCer) can protect against ca
64 rness innate immunity to fight cancer, alpha-galactosylceramide (alpha-GalCer) has been used to activ
65 The invariant NKT (iNKT) cell ligand alpha-galactosylceramide (alpha-GalCer) holds great promise in
67 KT cells in response to the NKT ligand alpha-galactosylceramide (alpha-GalCer) in both healthy donors
68 e third trimester by administration of alpha-galactosylceramide (alpha-GalCer) induced late PTB and n
69 nistration of the synthetic glycolipid alpha-galactosylceramide (alpha-GalCer) induces long-term NKT
71 r T (iNKT)-cells with the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the developme
78 dministration of the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) or the sphingosine-tru
79 chain recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the MHC c
80 cells recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the MHC c
81 )14 NKT cells by the glycosphingolipid alpha-galactosylceramide (alpha-GalCer) protects susceptible m
82 llographic and biophysical analyses of alpha-galactosylceramide (alpha-GalCer) recognition by a human
84 f mouse iNKT cells with the glycolipid alpha-galactosylceramide (alpha-GalCer) results in the acquisi
85 s activated with the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) stimulate a wide array
86 ing a tumor cell vaccine incorporating alpha-galactosylceramide (alpha-GalCer) that targets the immun
87 hat the addition of agonist glycolipid alpha-galactosylceramide (alpha-GalCer) to a fetal thymic orga
88 ansgenic mice by a single injection of alpha-galactosylceramide (alpha-GalCer), a glycolipid antigen
91 that a combination of vorinostat with alpha-galactosylceramide (alpha-GalCer), an IFN-gamma-inducing
92 s induced by concanavalin A (ConA) and alpha-galactosylceramide (alpha-GalCer), and hepatotoxin-media
93 14(+) TCR to CD1d requires the agonist alpha-galactosylceramide (alpha-GalCer), as opposed to the non
94 (NKT) cells by the glycolipid ligand, alpha-galactosylceramide (alpha-GalCer), causes bystander acti
95 The most powerful iNKT cell antigen is alpha-galactosylceramide (alpha-GalCer), derived from the mari
96 hetic glycolipid agonist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the developm
97 es of malaria parasites, a glycolipid, alpha-galactosylceramide (alpha-GalCer), known to selectively
98 mation, the effects of the glycolipid, alpha-galactosylceramide (alpha-GalCer), on dextran sodium sul
100 h as the marine sponge-derived reagent alpha-galactosylceramide (alpha-GalCer), results in the rapid
101 nist that is significantly weaker than alpha-galactosylceramide (alpha-GalCer), the most potent known
102 ptor (TCR) specific for the lipoglycan alpha-galactosylceramide (alpha-GalCer), which is presented by
103 ural killer T (NKT) cell superagonist, alpha-galactosylceramide (alpha-GalCer), which stimulates a wi
104 newly engineered antibody specific for alpha-galactosylceramide (alpha-GalCer)-human CD1d (hCD1d) com
106 n vivo administration of GD3 inhibited alpha-galactosylceramide (alpha-GalCer)-induced NKT cell activ
107 human NKT cell clones generated using alpha-galactosylceramide (alpha-GalCer)-loaded CD1d tetramers.
109 Remarkably NKT cells activated with alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells
110 escribe an atypical population of CD1d-alpha-galactosylceramide (alpha-GalCer)-reactive human NKT cel
111 of induction of IFN-gamma and IL-4 by alpha-galactosylceramide (alpha-GalCer)-stimulated liver NKT c
119 ive delta/alphabeta T cells recognized alpha-galactosylceramide (alpha-GalCer); however, their fine s
122 ion of NKT cells with the CD1d ligand (alpha-galactosylceramide [alpha-GC]) at the time of immunizati
124 R Jalpha281(-/-) (NKT cell deficient), alpha-galactosylceramide (alphaGalCer) (anergized NKT cells) i
126 ed presentation of NKT cell activating alpha galactosylceramide (alphaGalCer) analogs that give predo
128 iller T cells by using the CD1d ligand alpha-galactosylceramide (alphaGalCer) induces pregnancy loss
130 cell receptor (TCR)-specific reagents alpha-galactosylceramide (alphaGalCer) loaded CD1d-tetramers a
131 arine sponge-derived glycosphingolipid alpha-galactosylceramide (alphaGalCer) presented by the CD1d p
132 , strong activation of iNKT cells with alpha-galactosylceramide (alphaGalCer) reportedly induces a hy
133 stricted invariant NKT (iNKT) cells by alpha-galactosylceramide (alphaGalCer) significantly suppresse
135 he natural killer T (NKT) cell ligand, alpha-galactosylceramide (alphaGalCer), ameliorates autoimmune
136 esponses to CD1d-restricted glycolipid alpha-galactosylceramide (alphaGalCer), anti-CD3 antibody, and
137 as the prototypic NKT cell antagonist alpha-galactosylceramide (alphaGalCer), is currently being eva
138 etramers of mouse CD1d1 complexed with alpha-galactosylceramide (alphaGalCer), the antigen recognized
139 chemical structure to the well-studied alpha-galactosylceramide (alphaGalCer), with the only change b
140 (iNKT) as defined by staining with an alpha-galactosylceramide (alphaGalCer)-loaded CD1d-tetramer.
143 lipid variants of the NKT cell antigen alpha-galactosylceramide (alphaGC) exhibit decreased potency a
144 vants monophosphoryl lipid A (MPLA) or alpha-galactosylceramide (alphaGC) failed to elicit responses.
145 nvariant NKT (iNKT) immune cell ligand alpha-galactosylceramide (alphaGC) may offer novel tools for c
146 ndent and -independent activation with alpha-galactosylceramide (alphaGC) or IL-18 plus IL-12, respec
149 istration of a pegylated derivative of alpha-galactosylceramide (alphaGCPEG) with an antigen, even in
150 GalCer), as opposed to the nonantigenic beta-galactosylceramide, although both Ags bind to CD1d, indi
152 ntestinal (jejunal) epithelial cells express galactosylceramide, an alternative primary receptor for
155 cted with CVB3 and treated with either alpha-galactosylceramide, an NKT cell-specific ligand, or vehi
156 a7(+) NKT cells from mice, whereas the alpha-galactosylceramide analog OCH, with a truncated sphingos
157 that specifically activate NKT cells (alpha-GalactosylCeramide and a Sphingomonas bacterial glycolip
158 uch as an alpha-linked monosaccharide (alpha-galactosylceramide and alpha-galactosyldiacylglycerol) a
159 the use of CD1d tetramers loaded with alpha-galactosylceramide and antibodies specific to the invari
160 ncreasing emission intensity of anthrylvinyl-galactosylceramide and decreasing emission intensity of
161 of myelin-related glycosphingolipids (GSLs): galactosylceramide and galactosylsphingosine and sulfati
162 these mice, which failed to respond to alpha-galactosylceramide and which therefore were not classica
164 tly in brain because the major myelin lipids galactosylceramides and sulfatides contain 2-hydroxy fat
166 duction in response to the CD1d ligand alpha-galactosylceramide, and in NKT cell IFN-gamma production
167 ha-and beta-chains, does not recognize alpha-galactosylceramide, and is referred to as diverse NKT (d
168 dation made by this TCR in recognizing alpha-galactosylceramide, and it can be assumed that the most
170 tudies using synthetic pharmacological alpha-galactosylceramides, and the recent discovery of microbi
171 ,2-dilauroyl-sn-glycero-3-phosphocholine and galactosylceramide; and 4), binding of cholera-toxin B s
172 cells that recognize the prototypical alpha-galactosylceramide antigen, whereas the other major grou
173 h the CD1d-exposed portions of OCH and alpha-galactosylceramide are identical, structural analysis in
176 n of iNKT cells by a specific agonist, alpha-galactosylceramide, at the time of infection inhibited t
177 ransfer assay involving anthrylvinyl-labeled galactosylceramide (AV-GalCer) and perylenoyl-labeled tr
178 failed to respond to the model antigen alpha-galactosylceramide because of an intrinsic defect in the
179 he behavior was consistent with anthrylvinyl-galactosylceramide being transferred from donor to accep
180 w discovered another ceramide compound, beta-galactosylceramide (betaGalCer) (C12), that efficiently
181 investigated the intervesicular transfer of galactosylceramide between unilamellar bilayer vesicles
182 s also the most efficient in mediating alpha-galactosylceramide binding to recombinant plate-bound CD
183 omopolymer, identified residues that abolish galactosylceramide binding, phosphatidylcholine binding,
184 B subunit of cholera toxin to the conserved galactosylceramide-binding domain (including the ELDKWA-
189 mbination of GH-DT adjuvanted with the alpha-galactosylceramide C34 has the highest enhancement of an
190 1d-restricted T cells (NKT cells) with alpha-galactosylceramide caused diminished intestinal coloniza
192 ked decline in the percentage of CD3(+)alpha-galactosylceramide CD1d tetramer(+) cells in the mouse C
193 bset of NK T cells, which did not bind alpha-galactosylceramide-CD1d tetramers, was resistant to the
194 or [TCR] and can be detected using the alpha-galactosylceramide/CD1d tetramer) and type II (express d
195 in LacCer-cholesterol mixtures compared with galactosylceramide-cholesterol and sphingomyelin-cholest
199 glycosyl acceptor in the synthesis of alpha-galactosylceramide derivatives, was also readily prepare
201 ning globotriaosylceramide (Gb3Cer), but not galactosylceramide, dose-dependently prolonged clotting
202 n with these peptides and the adjuvant alpha-galactosylceramide elicits systemic and mucosal T-cell r
203 tivation of NKT cells by lipid agonist alpha-galactosylceramide enhances alternative macrophage polar
204 ike T (NKT) cells with the CD1d ligand alpha-galactosylceramide enhances T-dependent humoral immune r
207 -oleoyl-phosphatidylcholine vesicles shifted galactosylceramide from the inner to the outer leaflet.
208 e, to a glycolipid tentatively identified as galactosylceramide (Gal beta 1-1Cer) in the lipid extrac
210 atographically separated from their isobaric galactosylceramide (GalCer) counterparts using normal ph
212 ide (LacCer), glucosylceramide (GlcCer), and galactosylceramide (GalCer) has been quantitatively meas
213 d adhesion energy of the membrane glycolipid galactosylceramide (GalCer) were studied by osmotic stre
215 ng a long-chain saturated glycosphingolipid, galactosylceramide (GalCer), and cholesterol at room tem
217 Ls) that is enriched in lipids, specifically galactosylceramides (GalCer) originated at the endoplasm
218 drocytes and is responsible for synthesizing galactosylceramides (GalCer) that play an important role
220 d triglycosylceramides were characterized as galactosylceramide, glucosylceramide, lactosylceramide,
221 ed T-bet expression and in response to alpha-galactosylceramide, had deficient interferon-gamma expre
223 nvestigate the transmembrane distribution of galactosylceramide in phospholipid small unilamellar ves
225 CD1d-restricted NKT cells activated by alpha-galactosylceramide in young but not older dnTGFbetaRII m
226 stribution of a monohexosylceramide, such as galactosylceramide, in 1-palmitoyl-2-oleoyl-phosphatidyl
227 NZW)F(1) mice in vivo or in vitro with alpha-galactosylceramide indicated that the immunoregulatory r
228 the liver and protects from Con A- and alpha-galactosylceramide-induced hepatitis, both of which requ
229 variant (i)NKT cells with the model Ag alpha-galactosylceramide induces rapid production of multiple
230 t intrahepatic NK T cells activated by alpha-galactosylceramide inhibit hepatitis B virus replication
231 wild-type mice, IL-4 levels induced by alpha-galactosylceramide injection could be inhibited by a mAb
233 ng two forms of the NKT cell activator alpha-galactosylceramide into live BCG organisms, and the impa
237 I NKT cells, which can be detected by alpha-galactosylceramide-loaded CD1d tetramers, and less-studi
239 yeloma with 3 cycles of combination of alpha-galactosylceramide-loaded monocyte-derived dendritic cel
240 there was no increase in cells binding alpha-galactosylceramide-loaded tetramers, and alpha-galactosy
244 n iNKT cells are activated, whether by alpha-galactosylceramide or during IAV infection, iNKT cells i
245 cles of GlcCer, LacCer, or Gb(3)Cer, but not galactosylceramide or globotetraosylceramide, dose depen
246 mplexes from vesicles containing glycolipid (galactosylceramide or lactosylceramide) or from monosial
247 tracheal transfer of OVA-pulsed or OVA-alpha-galactosylceramide (OVA/alphaGalCer)-pulsed bone marrow-
249 oreactivity despite high reactivity to alpha-galactosylceramide presented by CD1d (alpha-GalCer/CD1d)
250 production of iNKT cells stimulated by alpha-galactosylceramide presented by CD1d+ Schwann cells show
252 pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increa
254 t, when NAD is injected into Con A- or alpha-galactosylceramide-primed mice, liver injury is exacerba
255 NK T (iNKT) cells with the glycolipid alpha-galactosylceramide promotes CD8(+) cytotoxic T cell resp
256 vation of NKT cells by the CD1d ligand alpha-galactosylceramide protects susceptible mice from tuberc
259 tant to iNKT cell-dependent lysis than alpha-galactosylceramide-pulsed DCs due to the weaker affinity
260 rated/secreted cytokine in response to alpha-galactosylceramide-pulsed PBMCs; tetramer-staining T cel
261 those that are mouse CD1 dependent and alpha-galactosylceramide reactive and those that are not, were
262 XCR4-tropic viral strains is mediated by the galactosylceramide receptor and the CXCR4 chemokine core
268 l(alpha1-->2)GalCer (Gal, galactose; GalCer, galactosylceramide), required removal of the terminal su
270 latively small amounts of incorporated alpha-galactosylceramide retained the ability to robustly acti
271 c cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses ongoing chronic and relapsi
272 Interfacial line tension measurements of galactosylceramide-rich domains track with our previousl
275 yperresponsive to anti-CD3, Con A, and alpha-galactosylceramide stimulation and secrete higher levels
276 ation and production of cytokines upon alpha-galactosylceramide stimulation in vitro and in vivo, and
279 the effect of increased sulfated content of galactosylceramides (sulfatides) on the regulation of PD
280 ication of only one glucosylceramide and one galactosylceramide synthase, both beta-transferases, in
281 antigens, including multiple forms of alpha-galactosylceramide that stimulate widely divergent cytok
282 t, following secondary activation with alpha-galactosylceramide, the behavior of iNKT cells is altere
283 sites within these antigens, including alpha-galactosylceramide, the structurally similar alpha-galac
284 stimulation with KRN7000, a synthetic alpha-galactosylceramide, they produce a vast amount of cytoki
285 reated with the iNKT cell superagonist alpha-galactosylceramide through a process involving enhanced
289 binding of an exogenous lipid antigen, alpha-galactosylceramide, to CD1d in the endocytic pathway.
290 Importantly, in vivo administration of alpha-galactosylceramide triggered a rapid IL-17 response in t
291 6e potently inhibits both anti-CD3 and alpha-galactosylceramide-triggered production of IFN-gamma by
293 variant T-cell receptor and react with alpha-galactosylceramide; type II NKT cells use diverse T-cell
295 ansion with a CD1d-presented lipid Ag (alpha-galactosylceramide) was diminished compared with healthy
297 studies using the iNKT-specific ligand alpha-galactosylceramide, which causes mild hepatitis in the m
298 mice did not respond to the lipoglycan alpha-galactosylceramide, which is presented by mouse CD1 to V
299 icably contains only a half-normal amount of galactosylceramide, which may account for the mild clini
300 ells were stained by tetramers of CD1d/alpha-galactosylceramide, which specifically identify the prev
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