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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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