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