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1 t needing the iNKT cell agonist ligand alpha-galactosylceramide.
2 ponsive to activation with the antigen alpha-galactosylceramide.
3 ed T cells cross-reacting against CD1d-alpha-galactosylceramide.
4 compared to a slight increase in males after galactosylceramide.
5 h glycolipid Ags, such as the model Ag alpha-galactosylceramide.
6 on than the invariant NKT cell agonist alpha-galactosylceramide.
7 ty than the most potent agonist known, alpha-galactosylceramide.
8 n almost identical fatty acyl chain as alpha-galactosylceramide.
9  prototypical type I NKT cell agonist, alpha-galactosylceramide.
10 sing the invariant NKT-specific ligand alpha-galactosylceramide.
11 ctivation of Valpha14 iNKT cells using alpha-galactosylceramide.
12 ivo and in vitro after activation with alpha-galactosylceramide.
13 stimulatory invariant NKT cell agonist alpha-galactosylceramide.
14 1d-dependent manner in the presence of alpha-galactosylceramide.
15 in intact lymphoid tissues, we studied alpha-galactosylceramide.
16 on of natural killer T cells by ligand alpha-galactosylceramide.
17 o achieve high affinity recognition of alpha-galactosylceramide.
18 rations after NKT cell activation with alpha-galactosylceramide.
19 NKT cell agonist, before they received alpha-galactosylceramide.
20 ferative defect after stimulation with alpha-galactosylceramide.
21  unique GSLs structurally derived from alpha-galactosylceramide.
22  following activation with CD1d ligand alpha-galactosylceramide.
23 e II NKT cells, which do not recognize alpha-galactosylceramide.
24 vision of a defined exogenous antigen, alpha-galactosylceramide.
25         Since the discovery in 1995 of alpha-galactosylceramide 1 (alpha-GalCer), also known as KRN70
26 ree novel subspecies of sphingolipids, alpha-galactosylceramides, 4,5-dihydroceramides, and 1-deoxysp
27 of the transbilayer distribution of [6-(13)C]galactosylceramide (99.8% isotopic enrichment) was achie
28     The fyn(-/-) NK T cells respond to alpha-galactosylceramide, a ligand recognized by NK T cells, a
29       Early treatment of NOD mice with alpha-galactosylceramide, a potent NK T cell activator, reduce
30    In addition, injection of mice with alpha-galactosylceramide, a specific glycolipid agonist of iNK
31                  The administration of alpha-galactosylceramide, a strong NK T-cell agonist, increase
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
35               Intravenous injection of alpha-galactosylceramide activated NKT1 cells with vascular ac
36 -gamma and IL-4 production, while oral alpha-galactosylceramide activated NKT2 cells in the mesenteri
37                     Blocking 4-1BBL in alpha-galactosylceramide-activated iNKT-monocyte cocultures re
38 he addition of either TiterMax Gold or alpha-galactosylceramide adjuvant, though adjuvant reduced cel
39 he addition of either TiterMax Gold or alpha-galactosylceramide adjuvant.
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
44 nize CD1d-restricted lipid Ags such as alpha-galactosylceramide (alpha GalCer).
45 y the marine sponge-derived glycolipid alpha-galactosylceramide (alpha GalCer).
46       Although the synthetic antigen alpha-D-galactosylceramide (alpha-D-GalCer) stimulates all Va14J
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 ecombinant CD1d protein complexed with alpha-galactosylceramide (alpha-GalCer) and quantitated hCD1d
55  of cytokine production in response to alpha-galactosylceramide (alpha-GalCer) and reduced iNKT cell-
56             CD1d tetramers loaded with alpha-galactosylceramide (alpha-GalCer) bind selectively to mo
57 en the highly potent synthetic antigen alpha-galactosylceramide (alpha-GalCer) binds CD1d.
58 hat recognition of glycolipids such as alpha-galactosylceramide (alpha-GalCer) by the NKT cell TCR (N
59 t NKT (iNKT) cells by the superagonist alpha-galactosylceramide (alpha-GalCer) can protect against ca
60           Activation of NKT cells with alpha-galactosylceramide (alpha-GalCer) causes liver injury th
61                         The glycolipid alpha-galactosylceramide (alpha-GalCer) has been shown to bind
62 rness innate immunity to fight cancer, alpha-galactosylceramide (alpha-GalCer) has been used to activ
63   The invariant NKT (iNKT) cell ligand alpha-galactosylceramide (alpha-GalCer) holds great promise in
64                      Administration of alpha-galactosylceramide (alpha-GalCer) in animals enhances an
65 KT cells in response to the NKT ligand alpha-galactosylceramide (alpha-GalCer) in both healthy donors
66 e third trimester by administration of alpha-galactosylceramide (alpha-GalCer) induced late PTB and n
67 nistration of the synthetic glycolipid alpha-galactosylceramide (alpha-GalCer) induces long-term NKT
68                 NKT cell activation by alpha-galactosylceramide (alpha-GalCer) inhibits autoimmune di
69 r T (iNKT)-cells with the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the developme
70 lopment of AHR after administration of alpha-galactosylceramide (alpha-GalCer) intranasally.
71                         The glycolipid alpha-galactosylceramide (alpha-GalCer) is a potent and specif
72                                        alpha-Galactosylceramide (alpha-GalCer) is a potent NKT cell a
73                                        alpha-Galactosylceramide (alpha-GalCer) is an iNKT cell-specif
74                                        alpha-Galactosylceramide (alpha-GalCer) is the prototypic agon
75 dministration of the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) or the sphingosine-tru
76 chain recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the MHC c
77 llographic and biophysical analyses of alpha-galactosylceramide (alpha-GalCer) recognition by a human
78                                        alpha-Galactosylceramide (alpha-GalCer) represents a new class
79 f mouse iNKT cells with the glycolipid alpha-galactosylceramide (alpha-GalCer) results in the acquisi
80 s activated with the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) stimulate a wide array
81 ing a tumor cell vaccine incorporating alpha-galactosylceramide (alpha-GalCer) that targets the immun
82 hat the addition of agonist glycolipid alpha-galactosylceramide (alpha-GalCer) to a fetal thymic orga
83                                        Alpha-Galactosylceramide (alpha-Galcer), a specific agonist fo
84                                        alpha-Galactosylceramide (alpha-GalCer), a specific ligand for
85  that a combination of vorinostat with alpha-galactosylceramide (alpha-GalCer), an IFN-gamma-inducing
86 s induced by concanavalin A (ConA) and alpha-galactosylceramide (alpha-GalCer), and hepatotoxin-media
87 14(+) TCR to CD1d requires the agonist alpha-galactosylceramide (alpha-GalCer), as opposed to the non
88  (NKT) cells by the glycolipid ligand, alpha-galactosylceramide (alpha-GalCer), causes bystander acti
89 The most powerful iNKT cell antigen is alpha-galactosylceramide (alpha-GalCer), derived from the mari
90 hetic glycolipid agonist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the developm
91       The prototypical NKT cell ligand alpha-galactosylceramide (alpha-GalCer), originally isolated f
92 h as the marine sponge-derived reagent alpha-galactosylceramide (alpha-GalCer), results in the rapid
93 nist that is significantly weaker than alpha-galactosylceramide (alpha-GalCer), the most potent known
94 ural killer T (NKT) cell superagonist, alpha-galactosylceramide (alpha-GalCer), which stimulates a wi
95 newly engineered antibody specific for alpha-galactosylceramide (alpha-GalCer)-human CD1d (hCD1d) com
96 including spontaneous, OVA-induced and alpha-galactosylceramide (alpha-GalCer)-induced AHR.
97 n vivo administration of GD3 inhibited alpha-galactosylceramide (alpha-GalCer)-induced NKT cell activ
98  human NKT cell clones generated using alpha-galactosylceramide (alpha-GalCer)-loaded CD1d tetramers.
99            Similar to human NKT cells, alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells
100    Remarkably NKT cells activated with alpha-galactosylceramide (alpha-GalCer)-pulsed dendritic cells
101 escribe an atypical population of CD1d-alpha-galactosylceramide (alpha-GalCer)-reactive human NKT cel
102  of induction of IFN-gamma and IL-4 by alpha-galactosylceramide (alpha-GalCer)-stimulated liver NKT c
103 nd lung CD1d-activated iNKT cells with alpha-galactosylceramide (alpha-GalCer).
104 tful using the CD1d-binding glycolipid alpha-galactosylceramide (alpha-GalCer).
105  of potent, exogenous ligands, such as alpha-galactosylceramide (alpha-GalCer).
106 er injury after in vivo challenge with alpha-galactosylceramide (alpha-GalCer).
107 itic cells pulsed with the NKT ligand, alpha-galactosylceramide (alpha-GalCer).
108  and respond to glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer).
109 ntation of the CD1-restricted antigen, alpha-galactosylceramide (alpha-GalCer).
110 he natural killer T (NKT)-cell agonist alpha-galactosylceramide (alpha-GalCer).
111 ive delta/alphabeta T cells recognized alpha-galactosylceramide (alpha-GalCer); however, their fine s
112 ed with the CD1d-binding glycolipid Ag alpha-galactosylceramide (alpha-GC).
113        The phytosphingosine-containing alpha-galactosylceramides (alpha-GalCers), KRN7000 and OCH, ha
114 ion of NKT cells with the CD1d ligand (alpha-galactosylceramide [alpha-GC]) at the time of immunizati
115 asured ex vivo and then incubated with alpha-galactosylceramide (alphaGal) and milk-SL.
116 R Jalpha281(-/-) (NKT cell deficient), alpha-galactosylceramide (alphaGalCer) (anergized NKT cells) i
117                    Here we report that alpha-galactosylceramide (alphaGalCer) activated NKT cells pos
118 ed presentation of NKT cell activating alpha galactosylceramide (alphaGalCer) analogs that give predo
119 KT cells by cognate glycolipid antigen alpha-galactosylceramide (alphaGalCer) and measured B cell act
120 itu by studying the adjuvant action of alpha-galactosylceramide (alphaGalCer) in mice.
121 iller T cells by using the CD1d ligand alpha-galactosylceramide (alphaGalCer) induces pregnancy loss
122           The marine sponge glycolipid alpha-galactosylceramide (alphaGalCer) is the proto-typic NKT
123  cell receptor (TCR)-specific reagents alpha-galactosylceramide (alphaGalCer) loaded CD1d-tetramers a
124 arine sponge-derived glycosphingolipid alpha-galactosylceramide (alphaGalCer) presented by the CD1d p
125 , strong activation of iNKT cells with alpha-galactosylceramide (alphaGalCer) reportedly induces a hy
126 stricted invariant NKT (iNKT) cells by alpha-galactosylceramide (alphaGalCer) significantly suppresse
127                                        alpha-Galactosylceramide (alphaGalCer) stimulates NKT cells an
128 eumoniae, lipopolysaccharide (LPS), or alpha-galactosylceramide (alphaGalCer) to induce pneumonia, se
129 he natural killer T (NKT) cell ligand, alpha-galactosylceramide (alphaGalCer), ameliorates autoimmune
130 esponses to CD1d-restricted glycolipid alpha-galactosylceramide (alphaGalCer), anti-CD3 antibody, and
131  as the prototypic NKT cell antagonist alpha-galactosylceramide (alphaGalCer), is currently being eva
132 chemical structure to the well-studied alpha-galactosylceramide (alphaGalCer), with the only change b
133  (iNKT) as defined by staining with an alpha-galactosylceramide (alphaGalCer)-loaded CD1d-tetramer.
134 activated by the CD1d-restricted lipid alpha-galactosylceramide (alphaGalCer).
135 ctively stimulate NKT cells in vivo is alpha-galactosylceramide (alphaGalCer).
136 lipid variants of the NKT cell antigen alpha-galactosylceramide (alphaGC) exhibit decreased potency a
137 vants monophosphoryl lipid A (MPLA) or alpha-galactosylceramide (alphaGC) failed to elicit responses.
138 nvariant NKT (iNKT) immune cell ligand alpha-galactosylceramide (alphaGC) may offer novel tools for c
139 ndent and -independent activation with alpha-galactosylceramide (alphaGC) or IL-18 plus IL-12, respec
140                 Structural variants of alpha-galactosylceramide (alphaGC) that activate invariant nat
141                Single vaccination with alpha-galactosylceramide (alphaGC)-loaded A20 lymphoma cells e
142 istration of a pegylated derivative of alpha-galactosylceramide (alphaGCPEG) with an antigen, even in
143                                              Galactosylceramide also increased neuronal cell counts s
144 GalCer), as opposed to the nonantigenic beta-galactosylceramide, although both Ags bind to CD1d, indi
145                  Repeated injection of alpha-galactosylceramide, an agonistic ligand for natural kill
146 ntestinal (jejunal) epithelial cells express galactosylceramide, an alternative primary receptor for
147 cterial infection by administration of alpha-galactosylceramide, an iNKT cell agonist.
148 they produce IL-13 upon stimulation by alpha-galactosylceramide, an NK-T cell-specific antigen.
149 cted with CVB3 and treated with either alpha-galactosylceramide, an NKT cell-specific ligand, or vehi
150 a7(+) NKT cells from mice, whereas the alpha-galactosylceramide analog OCH, with a truncated sphingos
151  that specifically activate NKT cells (alpha-GalactosylCeramide and a Sphingomonas bacterial glycolip
152 uch as an alpha-linked monosaccharide (alpha-galactosylceramide and alpha-galactosyldiacylglycerol) a
153  the use of CD1d tetramers loaded with alpha-galactosylceramide and antibodies specific to the invari
154 of myelin-related glycosphingolipids (GSLs): galactosylceramide and galactosylsphingosine and sulfati
155 eramidase (GALC) removes beta-galactose from galactosylceramide and other sphingolipids.
156 ransformed into globoid cells by exposure to galactosylceramide and produce a more severe GLD phenoty
157 these mice, which failed to respond to alpha-galactosylceramide and which therefore were not classica
158 nvolved in the formation of myelin 2-hydroxy galactosylceramides and -sulfatides.
159 tly in brain because the major myelin lipids galactosylceramides and sulfatides contain 2-hydroxy fat
160 -3-phosphocholine), a solid phase component (galactosylceramide), and cholesterol.
161 duction in response to the CD1d ligand alpha-galactosylceramide, and in NKT cell IFN-gamma production
162 ha-and beta-chains, does not recognize alpha-galactosylceramide, and is referred to as diverse NKT (d
163 dation made by this TCR in recognizing alpha-galactosylceramide, and it can be assumed that the most
164 tion in vivo, the role of the GALC substrate galactosylceramide, and the origin of psychosine are poo
165 ased brain levels of cholesterol, sulfatide, galactosylceramide, and triglyceride.
166 tudies using synthetic pharmacological alpha-galactosylceramides, and the recent discovery of microbi
167 ,2-dilauroyl-sn-glycero-3-phosphocholine and galactosylceramide; and 4), binding of cholera-toxin B s
168  cells that recognize the prototypical alpha-galactosylceramide antigen, whereas the other major grou
169 h the CD1d-exposed portions of OCH and alpha-galactosylceramide are identical, structural analysis in
170 ith a short-chain synthetic variant of alpha-galactosylceramide at a resolution of 2.2 A.
171 f human CD1d in complex with synthetic alpha-galactosylceramide at a resolution of 3.0 A.
172 n of iNKT cells by a specific agonist, alpha-galactosylceramide, at the time of infection inhibited t
173 ransfer assay involving anthrylvinyl-labeled galactosylceramide (AV-GalCer) and perylenoyl-labeled tr
174 failed to respond to the model antigen alpha-galactosylceramide because of an intrinsic defect in the
175 w discovered another ceramide compound, beta-galactosylceramide (betaGalCer) (C12), that efficiently
176  investigated the intervesicular transfer of galactosylceramide between unilamellar bilayer vesicles
177 s also the most efficient in mediating alpha-galactosylceramide binding to recombinant plate-bound CD
178 omopolymer, identified residues that abolish galactosylceramide binding, phosphatidylcholine binding,
179  B subunit of cholera toxin to the conserved galactosylceramide-binding domain (including the ELDKWA-
180                         The glycolipid alpha-galactosylceramide binds with high affinity to CD1d and
181 ted catabolically through the deacylation of galactosylceramide by acid ceramidase (ACDase).
182 ansport and is required for the breakdown of galactosylceramide by beta-galactosylceramidase.
183  is indispensable for in vivo degradation of galactosylceramide by GALC.
184  resulted in the lowest recognition of alpha-galactosylceramide by NKT cells.
185 mbination of GH-DT adjuvanted with the alpha-galactosylceramide C34 has the highest enhancement of an
186 1d-restricted T cells (NKT cells) with alpha-galactosylceramide caused diminished intestinal coloniza
187 ls increase, and further activation by alpha-galactosylceramide causes lethal liver injury.
188 ked decline in the percentage of CD3(+)alpha-galactosylceramide CD1d tetramer(+) cells in the mouse C
189 bset of NK T cells, which did not bind alpha-galactosylceramide-CD1d tetramers, was resistant to the
190 or [TCR] and can be detected using the alpha-galactosylceramide/CD1d tetramer) and type II (express d
191 in LacCer-cholesterol mixtures compared with galactosylceramide-cholesterol and sphingomyelin-cholest
192 R for CD1d/ threitolceramide than CD1d/alpha-galactosylceramide complexes.
193                                  Using alpha-galactosylceramide-containing CD1d tetramers to detect V
194 baseline AHR and, when challenged with alpha-GalactosylCeramide, demonstrated even greater AHR.
195  glycosyl acceptor in the synthesis of alpha-galactosylceramide derivatives, was also readily prepare
196 lactosylceramide-loaded tetramers, and alpha-galactosylceramide did not induce IL-13 secretion.
197 n with these peptides and the adjuvant alpha-galactosylceramide elicits systemic and mucosal T-cell r
198 tivation of NKT cells by lipid agonist alpha-galactosylceramide enhances alternative macrophage polar
199 ike T (NKT) cells with the CD1d ligand alpha-galactosylceramide enhances T-dependent humoral immune r
200 in films, but are somewhat more elastic than galactosylceramide films.
201 ated CD1d was functional in presenting alpha-galactosylceramide for iNKT cell expansion.
202 es and facilitating anterograde transport of galactosylceramide from Golgi to lipid rafts.
203 -oleoyl-phosphatidylcholine vesicles shifted galactosylceramide from the inner to the outer leaflet.
204      The myelin sheath is highly enriched in galactosylceramide (GalCer) and its sulfated derivative
205 atographically separated from their isobaric galactosylceramide (GalCer) counterparts using normal ph
206              Mucosal epithelial cell surface galactosylceramide (Galcer) has been postulated to be a
207 ide (LacCer), glucosylceramide (GlcCer), and galactosylceramide (GalCer) has been quantitatively meas
208                                              Galactosylceramide (GalCer), a glycosphingolipid, is bel
209 ng a long-chain saturated glycosphingolipid, galactosylceramide (GalCer), and cholesterol at room tem
210 consisting of phosphatidylcholine (POPC) and galactosylceramide (GalCer).
211 Ls) that is enriched in lipids, specifically galactosylceramides (GalCer) originated at the endoplasm
212 drocytes and is responsible for synthesizing galactosylceramides (GalCer) that play an important role
213 d triglycosylceramides were characterized as galactosylceramide, glucosylceramide, lactosylceramide,
214 ed T-bet expression and in response to alpha-galactosylceramide, had deficient interferon-gamma expre
215 3'-sulfolactose derivative and 3'-sulfo-beta-galactosylceramide, have been accomplished.
216 ure dendritic cells in the presence of alpha-galactosylceramide, IL-2, and IL-15.
217                                              Galactosylceramide improved behavioral, neuropathologica
218 nvestigate the transmembrane distribution of galactosylceramide in phospholipid small unilamellar ves
219 CD1d-restricted NKT cells activated by alpha-galactosylceramide in young but not older dnTGFbetaRII m
220 stribution of a monohexosylceramide, such as galactosylceramide, in 1-palmitoyl-2-oleoyl-phosphatidyl
221                   Injection of WT with alpha-galactosylceramide increased removal of senescent hepato
222                                              Galactosylceramide increased the lifespan of affected mi
223 NZW)F(1) mice in vivo or in vitro with alpha-galactosylceramide indicated that the immunoregulatory r
224 the liver and protects from Con A- and alpha-galactosylceramide-induced hepatitis, both of which requ
225 variant (i)NKT cells with the model Ag alpha-galactosylceramide induces rapid production of multiple
226 wild-type mice, IL-4 levels induced by alpha-galactosylceramide injection could be inhibited by a mAb
227                   Moreover, repetitive alpha-galactosylceramide injection of mice induced IL-21 but d
228 ng two forms of the NKT cell activator alpha-galactosylceramide into live BCG organisms, and the impa
229 p120 (K(d), 35.4 nM), CD4 (K(d), 31 nM), and galactosylceramide (K(d), 24.1 nM).
230 r is relatively low compared with CD1d-alpha-galactosylceramide (KD of 19-26 muM versus 1 muM).
231                              A form of alpha-galactosylceramide, KRN7000, activates CD1d-restricted V
232 rols, iNKT cells were enumerated using alpha-galactosylceramide-loaded CD1d tetramers and subsequentl
233  I NKT cells, which can be detected by alpha-galactosylceramide-loaded CD1d tetramers, and less-studi
234                      These cells bound alpha-galactosylceramide-loaded CD1d tetramers, but exhibited
235 yeloma with 3 cycles of combination of alpha-galactosylceramide-loaded monocyte-derived dendritic cel
236 there was no increase in cells binding alpha-galactosylceramide-loaded tetramers, and alpha-galactosy
237 rime CD8(+) T cells without relying on alpha-galactosylceramide loading.
238                                The amount of galactosylceramide localized in the inner leaflet decrea
239                                        In PI/galactosylceramide mixtures, DAG may exert its activatio
240                  Additionally, the impact of galactosylceramide on ceramide synthesis enzymes is docu
241 n iNKT cells are activated, whether by alpha-galactosylceramide or during IAV infection, iNKT cells i
242 mplexes from vesicles containing glycolipid (galactosylceramide or lactosylceramide) or from monosial
243                  A group of 72 mice received galactosylceramide or vehicle for 40 weeks.
244 tracheal transfer of OVA-pulsed or OVA-alpha-galactosylceramide (OVA/alphaGalCer)-pulsed bone marrow-
245                  The data show that [6-(13)C]galactosylceramide prefers (70%) the inner leaflet of ph
246 production of iNKT cells stimulated by alpha-galactosylceramide presented by CD1d+ Schwann cells show
247           Unlike in standard NOD mice, alpha-galactosylceramide pretreatment did not protect the CD38
248 pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs increa
249 T cells and only moderately stimulated alpha-galactosylceramide-primed invariant NKT cells.
250 t, when NAD is injected into Con A- or alpha-galactosylceramide-primed mice, liver injury is exacerba
251  NK T (iNKT) cells with the glycolipid alpha-galactosylceramide promotes CD8(+) cytotoxic T cell resp
252 vation of NKT cells by the CD1d ligand alpha-galactosylceramide protects susceptible mice from tuberc
253 tion upon stimulation with anti-CD3 or alpha-galactosylceramide-pulsed APCs.
254                   When cocultured with alpha-galactosylceramide-pulsed B cells, CD4(+) and DN iNKT ce
255 tant to iNKT cell-dependent lysis than alpha-galactosylceramide-pulsed DCs due to the weaker affinity
256 rated/secreted cytokine in response to alpha-galactosylceramide-pulsed PBMCs; tetramer-staining T cel
257 XCR4-tropic viral strains is mediated by the galactosylceramide receptor and the CXCR4 chemokine core
258 hydroxy moiety does not significantly affect galactosylceramide recognition.
259                         Treatment with alpha-galactosylceramide reduced the bacterial burden in the l
260                   Sulfatide accumulated, but galactosylceramide remained at WT levels, in the AB-/- m
261                                        alpha-Galactosylceramide represents a new class of vaccine adj
262             Whereas NKT stimulation by alpha-Galactosylceramide required CD1d expression by dendritic
263 l(alpha1-->2)GalCer (Gal, galactose; GalCer, galactosylceramide), required removal of the terminal su
264 ction has been found to be mediated by alpha-galactosylceramide-responsive type I NKT cells.
265                                              Galactosylceramide resulted in enhanced grip strength of
266 latively small amounts of incorporated alpha-galactosylceramide retained the ability to robustly acti
267 c cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses ongoing chronic and relapsi
268     Interfacial line tension measurements of galactosylceramide-rich domains track with our previousl
269                      Mice treated with alpha-galactosylceramide showed significantly reduced myocardi
270                  Oral vaccination with alpha-galactosylceramide shows enhanced fecal IgG1 titers in i
271                              Rare CD1d-alpha-galactosylceramide-specific T cells that do not express
272 yperresponsive to anti-CD3, Con A, and alpha-galactosylceramide stimulation and secrete higher levels
273 ation and production of cytokines upon alpha-galactosylceramide stimulation in vitro and in vivo, and
274 ination and secondary neuroinflammation from galactosylceramide storage in macrophages.
275                   The prototypical Ag, alpha-galactosylceramide, strongly activates human and mouse i
276                                     Sulfated galactosylceramides (sulfatides) are glycosphingolipids
277  the effect of increased sulfated content of galactosylceramides (sulfatides) on the regulation of PD
278                                The effect of galactosylceramide supplementation on Cln3 (Deltaex7/8)
279 he beneficial effects of long-term exogenous galactosylceramide supplementation on longevity, neurobe
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      However, repeated treatments with alpha-galactosylceramide, the prototypic glycolipid ligand of
284 sites within these antigens, including alpha-galactosylceramide, the structurally similar alpha-galac
285  stimulation with KRN7000, a synthetic alpha-galactosylceramide, they produce a vast amount of cytoki
286 reated with the iNKT cell superagonist alpha-galactosylceramide through a process involving enhanced
287 amine (DEN) to induce liver cancer and alpha-galactosylceramide to activate natural killer T (NKT) ce
288 tential and can present the glycolipid alpha-galactosylceramide to iNKT cells.
289 ipation in the CD1d Ag presentation of alpha-galactosylceramide to NK T cells is not necessary.
290 t impairment in the ability to present alpha-galactosylceramide to NKT cells.
291 binding of an exogenous lipid antigen, alpha-galactosylceramide, to CD1d in the endocytic pathway.
292 els as well as apoptosis rates were lower in galactosylceramide-treated Cln3 (Deltaex7/8) mice.
293 Importantly, in vivo administration of alpha-galactosylceramide triggered a rapid IL-17 response in t
294 6e potently inhibits both anti-CD3 and alpha-galactosylceramide-triggered production of IFN-gamma by
295       We demonstrate that injection of alpha-galactosylceramide triggers CD70 expression on splenic T
296 variant T-cell receptor and react with alpha-galactosylceramide; type II NKT cells use diverse T-cell
297 aroyl phosphatidylcholine, sphingomyelin, or galactosylceramide, used as substrates.
298               C-glycoside analogues of alpha-galactosylceramide were shown to activate both human and
299 studies using the iNKT-specific ligand alpha-galactosylceramide, which causes mild hepatitis in the m
300 ells were stained by tetramers of CD1d/alpha-galactosylceramide, which specifically identify the prev

 
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