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1 zing iNKT cell agonist, before they received alpha-galactosylceramide.
2 on with glycolipid Ags, such as the model Ag alpha-galactosylceramide.
3 nfection than the invariant NKT cell agonist alpha-galactosylceramide.
4 avidity than the most potent agonist known, alpha-galactosylceramide.
5 has an almost identical fatty acyl chain as alpha-galactosylceramide.
6 proliferative defect after stimulation with alpha-galactosylceramide.
7 ound using the invariant NKT-specific ligand alpha-galactosylceramide.
8 by coactivation of Valpha14 iNKT cells using alpha-galactosylceramide.
9 a in vivo and in vitro after activation with alpha-galactosylceramide.
10 ighly stimulatory invariant NKT cell agonist alpha-galactosylceramide.
11 n a CD1d-dependent manner in the presence of alpha-galactosylceramide.
12 nisms in intact lymphoid tissues, we studied alpha-galactosylceramide.
13 tivation of natural killer T cells by ligand alpha-galactosylceramide.
14 ain, to achieve high affinity recognition of alpha-galactosylceramide.
15 e alterations after NKT cell activation with alpha-galactosylceramide.
16 e five unique GSLs structurally derived from alpha-galactosylceramide.
17 ens: peptides or proteins and the glycolipid alpha-galactosylceramide.
18 igated following activation with CD1d ligand alpha-galactosylceramide.
19 ed type II NKT cells, which do not recognize alpha-galactosylceramide.
20 ot the prototypical type I NKT cell agonist, alpha-galactosylceramide.
21 by provision of a defined exogenous antigen, alpha-galactosylceramide.
22 without needing the iNKT cell agonist ligand alpha-galactosylceramide.
23 yporesponsive to activation with the antigen alpha-galactosylceramide.
24 stricted T cells cross-reacting against CD1d-alpha-galactosylceramide.
26 out three novel subspecies of sphingolipids, alpha-galactosylceramides, 4,5-dihydroceramides, and 1-d
33 trate that the downstream effects induced by alpha-galactosylceramide activated NK T cells on NK cell
35 rferon-gamma and IL-4 production, while oral alpha-galactosylceramide activated NKT2 cells in the mes
37 d by the addition of either TiterMax Gold or alpha-galactosylceramide adjuvant, though adjuvant reduc
39 antimicrobial immune response suggests that alpha-galactosylceramide administration could have a rol
40 the presence or absence of iNKT-cell agonist alpha-galactosylceramide, after which OTI T-cell priming
41 tation of the functional glycolipid antigen, alpha-galactosylceramide (alpha GalCer), to the mouse NK
42 iate a rapid reaction to the glycolipid drug alpha-galactosylceramide (alpha GalCer), which triggers
45 the third compound was the glycosphingolipid alpha-galactosylceramide (alpha-GalCer(Bf)), which is st
46 of iNKT through injection of iNKT activator alpha-galactosylceramide (alpha-GalCer) accelerates CCl(
47 alphabeta T lymphocytes, with use of mucosal alpha-galactosylceramide (alpha-GalCer) administration,
48 ine (alpha-GalPhyt) from which 6"-N-modified alpha-galactosylceramide (alpha-GalCer) analogues can be
49 cell receptor beta-chain repertoire and how alpha-galactosylceramide (alpha-GalCer) analogues induce
50 n vivo activation of V alpha 14 NKT cells by alpha-galactosylceramide (alpha-GalCer) and CD1d potenti
51 erably reduces CD1d-mediated presentation of alpha-galactosylceramide (alpha-galcer) and endogenous a
52 nition against altered glycolipid ligands of alpha-galactosylceramide (alpha-GalCer) and have determi
53 activation of NK T cells with the glycolipid alpha-galactosylceramide (alpha-GalCer) and myelin-react
54 sing recombinant CD1d protein complexed with alpha-galactosylceramide (alpha-GalCer) and quantitated
55 bsence of cytokine production in response to alpha-galactosylceramide (alpha-GalCer) and reduced iNKT
56 er (NK) T cells reactive with the glycolipid alpha-galactosylceramide (alpha-GalCer) are a distinct l
59 ught that recognition of glycolipids such as alpha-galactosylceramide (alpha-GalCer) by the NKT cell
60 variant NKT (iNKT) cells by the superagonist alpha-galactosylceramide (alpha-GalCer) can protect agai
63 To harness innate immunity to fight cancer, alpha-galactosylceramide (alpha-GalCer) has been used to
66 n of NKT cells in response to the NKT ligand alpha-galactosylceramide (alpha-GalCer) in both healthy
67 in the third trimester by administration of alpha-galactosylceramide (alpha-GalCer) induced late PTB
68 e administration of the synthetic glycolipid alpha-galactosylceramide (alpha-GalCer) induces long-ter
70 killer T (iNKT)-cells with the superagonist alpha-galactosylceramide (alpha-GalCer) inhibits the dev
71 e development of AHR after administration of alpha-galactosylceramide (alpha-GalCer) intranasally.
77 ough administration of the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) or the sphingosi
78 alpha-chain recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the
79 NK T cells recognize glycolipid Ags such as alpha-galactosylceramide (alpha-GalCer) presented by the
80 (alpha)14 NKT cells by the glycosphingolipid alpha-galactosylceramide (alpha-GalCer) protects suscept
81 crystallographic and biophysical analyses of alpha-galactosylceramide (alpha-GalCer) recognition by a
83 tion of mouse iNKT cells with the glycolipid alpha-galactosylceramide (alpha-GalCer) results in the a
84 -cells activated with the glycolipid ligand alpha-galactosylceramide (alpha-GalCer) stimulate a wide
85 eveloping a tumor cell vaccine incorporating alpha-galactosylceramide (alpha-GalCer) that targets the
86 port that the addition of agonist glycolipid alpha-galactosylceramide (alpha-GalCer) to a fetal thymi
87 man CD1 molecules can present the glycolipid alpha-galactosylceramide (alpha-GalCer) to NK T cells fr
89 bamoyl]cholesterol (DC-Chol) with or without alpha-galactosylceramide (alpha-GalCer) were produced by
90 HBV transgenic mice by a single injection of alpha-galactosylceramide (alpha-GalCer), a glycolipid an
93 e show that a combination of vorinostat with alpha-galactosylceramide (alpha-GalCer), an IFN-gamma-in
94 patitis induced by concanavalin A (ConA) and alpha-galactosylceramide (alpha-GalCer), and hepatotoxin
95 alpha 14(+) TCR to CD1d requires the agonist alpha-galactosylceramide (alpha-GalCer), as opposed to t
96 ller T (NKT) cells by the glycolipid ligand, alpha-galactosylceramide (alpha-GalCer), causes bystande
98 a synthetic glycolipid agonist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the de
99 r stages of malaria parasites, a glycolipid, alpha-galactosylceramide (alpha-GalCer), known to select
100 inflammation, the effects of the glycolipid, alpha-galactosylceramide (alpha-GalCer), on dextran sodi
102 s, such as the marine sponge-derived reagent alpha-galactosylceramide (alpha-GalCer), results in the
103 ay exquisite specificity for CD1d presenting alpha-galactosylceramide (alpha-GalCer), the extent of l
104 ll agonist that is significantly weaker than alpha-galactosylceramide (alpha-GalCer), the most potent
105 l receptor (TCR) specific for the lipoglycan alpha-galactosylceramide (alpha-GalCer), which is presen
106 nt natural killer T (NKT) cell superagonist, alpha-galactosylceramide (alpha-GalCer), which stimulate
107 and a newly engineered antibody specific for alpha-galactosylceramide (alpha-GalCer)-human CD1d (hCD1
108 thma, including spontaneous, OVA-induced and alpha-galactosylceramide (alpha-GalCer)-induced AHR.
109 tly, in vivo administration of GD3 inhibited alpha-galactosylceramide (alpha-GalCer)-induced NKT cell
110 sitive human NKT cell clones generated using alpha-galactosylceramide (alpha-GalCer)-loaded CD1d tetr
113 We describe an atypical population of CD1d-alpha-galactosylceramide (alpha-GalCer)-reactive human N
114 bition of induction of IFN-gamma and IL-4 by alpha-galactosylceramide (alpha-GalCer)-stimulated liver
124 -reactive delta/alphabeta T cells recognized alpha-galactosylceramide (alpha-GalCer); however, their
127 ctivation of NKT cells with the CD1d ligand (alpha-galactosylceramide [alpha-GC]) at the time of immu
129 analyzed presentation of NKT cell activating alpha galactosylceramide (alphaGalCer) analogs that give
130 B6.TCR Jalpha281(-/-) (NKT cell deficient), alpha-galactosylceramide (alphaGalCer) (anergized NKT ce
132 ted iNKT cells by cognate glycolipid antigen alpha-galactosylceramide (alphaGalCer) and measured B ce
134 ural killer T cells by using the CD1d ligand alpha-galactosylceramide (alphaGalCer) induces pregnancy
136 d of T cell receptor (TCR)-specific reagents alpha-galactosylceramide (alphaGalCer) loaded CD1d-tetra
137 the marine sponge-derived glycosphingolipid alpha-galactosylceramide (alphaGalCer) presented by the
138 owever, strong activation of iNKT cells with alpha-galactosylceramide (alphaGalCer) reportedly induce
139 D1d-restricted invariant NKT (iNKT) cells by alpha-galactosylceramide (alphaGalCer) significantly sup
141 cus pneumoniae, lipopolysaccharide (LPS), or alpha-galactosylceramide (alphaGalCer) to induce pneumon
142 with the natural killer T (NKT) cell ligand, alpha-galactosylceramide (alphaGalCer), ameliorates auto
143 kine responses to CD1d-restricted glycolipid alpha-galactosylceramide (alphaGalCer), anti-CD3 antibod
144 , such as the prototypic NKT cell antagonist alpha-galactosylceramide (alphaGalCer), is currently bei
145 cent tetramers of mouse CD1d1 complexed with alpha-galactosylceramide (alphaGalCer), the antigen reco
146 ar in chemical structure to the well-studied alpha-galactosylceramide (alphaGalCer), with the only ch
147 cells (iNKT) as defined by staining with an alpha-galactosylceramide (alphaGalCer)-loaded CD1d-tetra
150 rated lipid variants of the NKT cell antigen alpha-galactosylceramide (alphaGC) exhibit decreased pot
151 r adjuvants monophosphoryl lipid A (MPLA) or alpha-galactosylceramide (alphaGC) failed to elicit resp
152 the invariant NKT (iNKT) immune cell ligand alpha-galactosylceramide (alphaGC) may offer novel tools
153 R-dependent and -independent activation with alpha-galactosylceramide (alphaGC) or IL-18 plus IL-12,
156 -administration of a pegylated derivative of alpha-galactosylceramide (alphaGCPEG) with an antigen, e
159 since they produce IL-13 upon stimulation by alpha-galactosylceramide, an NK-T cell-specific antigen.
160 e infected with CVB3 and treated with either alpha-galactosylceramide, an NKT cell-specific ligand, o
161 ogical NKT cell activation using a synthetic alpha-galactosylceramide analog (KRN7000) restored local
162 y Vbeta7(+) NKT cells from mice, whereas the alpha-galactosylceramide analog OCH, with a truncated sp
163 tigens that specifically activate NKT cells (alpha-GalactosylCeramide and a Sphingomonas bacterial gl
164 ens, such as an alpha-linked monosaccharide (alpha-galactosylceramide and alpha-galactosyldiacylglyce
165 y with the use of CD1d tetramers loaded with alpha-galactosylceramide and antibodies specific to the
166 ls in these mice, which failed to respond to alpha-galactosylceramide and which therefore were not cl
167 ne production in response to the CD1d ligand alpha-galactosylceramide, and in NKT cell IFN-gamma prod
168 R) alpha-and beta-chains, does not recognize alpha-galactosylceramide, and is referred to as diverse
169 ccommodation made by this TCR in recognizing alpha-galactosylceramide, and it can be assumed that the
170 lls, studies using synthetic pharmacological alpha-galactosylceramides, and the recent discovery of m
171 (iNKT) cells that recognize the prototypical alpha-galactosylceramide antigen, whereas the other majo
172 lthough the CD1d-exposed portions of OCH and alpha-galactosylceramide are identical, structural analy
175 ivation of iNKT cells by a specific agonist, alpha-galactosylceramide, at the time of infection inhib
176 that failed to respond to the model antigen alpha-galactosylceramide because of an intrinsic defect
177 ut symbiont Bacteroides fragilis can produce alpha-galactosylceramides (BfaGCs), sphingolipids with i
178 n B was also the most efficient in mediating alpha-galactosylceramide binding to recombinant plate-bo
181 the combination of GH-DT adjuvanted with the alpha-galactosylceramide C34 has the highest enhancement
182 of Cd1d-restricted T cells (NKT cells) with alpha-galactosylceramide caused diminished intestinal co
183 T cells increase, and further activation by alpha-galactosylceramide causes lethal liver injury.
184 a marked decline in the percentage of CD3(+)alpha-galactosylceramide CD1d tetramer(+) cells in the m
185 y a subset of NK T cells, which did not bind alpha-galactosylceramide-CD1d tetramers, was resistant t
186 receptor [TCR] and can be detected using the alpha-galactosylceramide/CD1d tetramer) and type II (exp
189 rated baseline AHR and, when challenged with alpha-GalactosylCeramide, demonstrated even greater AHR.
190 l as a glycosyl acceptor in the synthesis of alpha-galactosylceramide derivatives, was also readily p
191 pha-galactosylceramide-loaded tetramers, and alpha-galactosylceramide did not induce IL-13 secretion.
193 ination with these peptides and the adjuvant alpha-galactosylceramide elicits systemic and mucosal T-
194 ng, activation of NKT cells by lipid agonist alpha-galactosylceramide enhances alternative macrophage
195 ller-like T (NKT) cells with the CD1d ligand alpha-galactosylceramide enhances T-dependent humoral im
197 ecreased T-bet expression and in response to alpha-galactosylceramide, had deficient interferon-gamma
199 patic CD1d-restricted NKT cells activated by alpha-galactosylceramide in young but not older dnTGFbet
201 NZB x NZW)F(1) mice in vivo or in vitro with alpha-galactosylceramide indicated that the immunoregula
202 ls in the liver and protects from Con A- and alpha-galactosylceramide-induced hepatitis, both of whic
203 of invariant (i)NKT cells with the model Ag alpha-galactosylceramide induces rapid production of mul
204 ed that intrahepatic NK T cells activated by alpha-galactosylceramide inhibit hepatitis B virus repli
205 In wild-type mice, IL-4 levels induced by alpha-galactosylceramide injection could be inhibited by
207 porating two forms of the NKT cell activator alpha-galactosylceramide into live BCG organisms, and th
208 eceptor is relatively low compared with CD1d-alpha-galactosylceramide (KD of 19-26 muM versus 1 muM).
210 d controls, iNKT cells were enumerated using alpha-galactosylceramide-loaded CD1d tetramers and subse
211 d type I NKT cells, which can be detected by alpha-galactosylceramide-loaded CD1d tetramers, and less
213 atic myeloma with 3 cycles of combination of alpha-galactosylceramide-loaded monocyte-derived dendrit
214 since there was no increase in cells binding alpha-galactosylceramide-loaded tetramers, and alpha-gal
216 When iNKT cells are activated, whether by alpha-galactosylceramide or during IAV infection, iNKT c
217 intratracheal transfer of OVA-pulsed or OVA-alpha-galactosylceramide (OVA/alphaGalCer)-pulsed bone m
218 nt autoreactivity despite high reactivity to alpha-galactosylceramide presented by CD1d (alpha-GalCer
219 okine production of iNKT cells stimulated by alpha-galactosylceramide presented by CD1d+ Schwann cell
221 gamma pathway and NKT cells by administering alpha-galactosylceramide-primed bone marrow-derived DCs
222 D4(+) T cells and only moderately stimulated alpha-galactosylceramide-primed invariant NKT cells.
223 ontrast, when NAD is injected into Con A- or alpha-galactosylceramide-primed mice, liver injury is ex
224 ariant NK T (iNKT) cells with the glycolipid alpha-galactosylceramide promotes CD8(+) cytotoxic T cel
225 c activation of NKT cells by the CD1d ligand alpha-galactosylceramide protects susceptible mice from
228 resistant to iNKT cell-dependent lysis than alpha-galactosylceramide-pulsed DCs due to the weaker af
229 roliferated/secreted cytokine in response to alpha-galactosylceramide-pulsed PBMCs; tetramer-staining
230 uding those that are mouse CD1 dependent and alpha-galactosylceramide reactive and those that are not
234 protection has been found to be mediated by alpha-galactosylceramide-responsive type I NKT cells.
235 ing relatively small amounts of incorporated alpha-galactosylceramide retained the ability to robustl
236 nthetic cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses ongoing chronic and r
240 are hyperresponsive to anti-CD3, Con A, and alpha-galactosylceramide stimulation and secrete higher
241 oliferation and production of cytokines upon alpha-galactosylceramide stimulation in vitro and in viv
243 olipid antigens, including multiple forms of alpha-galactosylceramide that stimulate widely divergent
244 ontrast, following secondary activation with alpha-galactosylceramide, the behavior of iNKT cells is
246 topic sites within these antigens, including alpha-galactosylceramide, the structurally similar alpha
247 diated stimulation with KRN7000, a synthetic alpha-galactosylceramide, they produce a vast amount of
248 mice treated with the iNKT cell superagonist alpha-galactosylceramide through a process involving enh
249 nitrosamine (DEN) to induce liver cancer and alpha-galactosylceramide to activate natural killer T (N
251 participation in the CD1d Ag presentation of alpha-galactosylceramide to NK T cells is not necessary.
253 r the binding of an exogenous lipid antigen, alpha-galactosylceramide, to CD1d in the endocytic pathw
255 ATL146e potently inhibits both anti-CD3 and alpha-galactosylceramide-triggered production of IFN-gam
257 emi-invariant T-cell receptor and react with alpha-galactosylceramide; type II NKT cells use diverse
258 vo expansion with a CD1d-presented lipid Ag (alpha-galactosylceramide) was diminished compared with h
260 ed by studies using the iNKT-specific ligand alpha-galactosylceramide, which causes mild hepatitis in
261 ta-/- mice did not respond to the lipoglycan alpha-galactosylceramide, which is presented by mouse CD
262 nt T cells were stained by tetramers of CD1d/alpha-galactosylceramide, which specifically identify th