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1 both antigen-specific CD4+ and CD8+ T cells (cross-presentation).
2 rnalization, CD40, was the most efficient at cross presentation.
3 n to MHC class I molecules, a process termed cross presentation.
4 the two conformational states to potentiate cross-presentation.
5 ated C-type lectin receptors fail to promote cross-presentation.
6 f which contributes to the fine-tuning of Ag cross-presentation.
7 d tumor immunogenicity and optimized antigen cross-presentation.
8 d mediates the power of DC efferocytosis and cross-presentation.
9 role of oxidized lipids in the regulation of cross-presentation.
10 to elucidate the mechanisms of TLR2-mediated cross-presentation.
11 trols phagosomal pH, a critical parameter in cross-presentation.
12 --that mediates DC efferocytosis and antigen cross-presentation.
13 ulation of nonoxidized lipids did not affect cross-presentation.
14 ctive of T-cell receptor affinity or antigen cross-presentation.
15 ell immunity to these pathogens necessitates cross-presentation.
16 ate naive CD8(+) T cells in a process termed cross-presentation.
17 teasomal degradation products and blocked Ag cross-presentation.
18 ose of a less pure LPS preparation inhibited cross-presentation.
19 to pure LPS abrogated its ability to enhance cross-presentation.
20 s of DC maturation on MHC class I-restricted cross-presentation.
21 strong as those induced exclusively through cross-presentation.
22 ose virus strains that are most dependent on cross-presentation.
23 class I loading in a process referred to as cross-presentation.
24 tor specialized for delivery of antigens for cross-presentation.
25 from internalized proteins, a process called cross-presentation.
26 nological function in dendritic cell (DC) Ag cross-presentation.
27 h the cytosolic from the vacuolar pathway of cross-presentation.
28 re them with lymph node resident DCs through cross-presentation.
29 some recruitment and enhance TAP-independent cross-presentation.
30 us (IAV)-peptides following either direct or cross-presentation.
31 T cells, but in vivo immunity still requires cross-presentation.
32 mic reticulum-phagosome traffic required for cross-presentation.
33 DCs are responsible for antigen exchange and cross-presentation.
34 thereby optimizing XCR1(+) DC maturation and cross-presentation.
35 lpha(+) dendritic cells (DCs) in exosomal Ag cross-presentation.
36 o draining lymph nodes, and enhances antigen cross-presentation.
37 and captured stable proteins permissive for cross-presentation.
38 te defects in both CD8 T cell activation and cross-presentation.
39 lar milieu on MHC-I through a process called cross-presentation.
40 I (MHC-I) molecules are the centerpieces of cross-presentation.
41 st be deployed to deliver Ag to pDCs for Ag (cross-)presentation.
42 ient (FcgammaR quadruple(-/-)) mice, and the cross-presentation ability of CD8alpha(+) DCs was not af
43 e investigated the mechanisms underlying the cross-presentation ability of IFN-DCs by studying the in
44 fy4 (-/-) mice with known defects in antigen cross-presentation, accumulated in joint tissue and the
47 l phagocytosis subsequently enhances antigen cross-presentation and activation of cyclic GMP-AMP synt
48 +) DCs led to cytokine production and robust cross-presentation and activation of tumor antigen-speci
49 nt cell death pathways may affect neoepitope cross-presentation and Ag recognition of cancer cells.
51 ype 1 dendritic cells that are essential for cross-presentation and CD8 T cell-mediated immunity agai
53 bulk large tumors, release tumor antigen for cross-presentation and cross-priming, release cancer-sup
55 ogel significantly enhanced antigen-specific cross-presentation and cytotoxic T lymphocyte (CTL) acti
56 ockade also potently suppressed both antigen cross-presentation and direct presentation of synthetic
57 organ-resident CD8(+) DCs are specialized at cross-presentation and have developed specific adaptatio
58 ings provide important insights into antigen cross-presentation and have implications for development
59 eeks of T cell-replete syngeneic HSCT led to cross-presentation and increased survival of lymphoma-be
60 istinct pathway that operates within DCs for cross-presentation and is required for the activation of
61 rmulations with peptide Ags stimulate strong cross-presentation and potent CD8 T cell responses assoc
62 are unique organ-resident APCs capable of Ag cross-presentation and subsequent tolerization of naive
65 processing of dead cell-derived antigens for cross-presentation and the induction of effective CD8(+)
66 3(+) mDCs are presented by both MHC class I (cross-presentation) and MHC class II to antigen-specific
68 cific T cells poorly, despite its long-lived cross-presentation, and T cells primed against the short
69 in TLR-induced dendritic cell activation and cross-presentation, and thus is vital in host defense.
72 riming and tumor rejection required tumor Ag cross-presentation, as evidenced by tumor outgrowth in K
73 wn as IFN-DCs, highly efficient in mediating cross-presentation, as well as the cross-priming of CD8(
75 es IC uptake and is essentially required for cross-presentation, but not for MHC class II Ag presenta
77 lysaccharide and interferon-gamma as well as cross-presentation by bone marrow-derived dendritic cell
81 cell responses were attributed to increased cross-presentation by DCs along with increased detection
84 ficking protein Rab39a is needed for optimal cross-presentation by dendritic cells in vitro and cross
85 educe IRAP-dependent but not ERAP1-dependent cross-presentation by dendritic cells with nanomolar eff
86 s and mediators, IgE-mediated tumour antigen cross-presentation by dendritic cells, as well as immuno
87 3(+) DCs and not BDCA-1(+) DCs show improved cross-presentation by FcgammaR targeting, as measured by
90 ontrast to classical spleen dendritic cells, cross-presentation by liver antigen-presenting cells was
91 f HA-1 long peptide resulted in efficient Ag cross-presentation by mDCs and pDCs, leading to strong e
92 ning the tyrosine signal but does not affect cross-presentation by MHC-I containing the HLA-C cytopla
94 in adaptor protein 1 (AP-1) is necessary for cross-presentation by MHC-I molecules containing a cytop
95 n contrast, AP-1 activity was not needed for cross-presentation by MHC-I molecules containing a human
98 ntigen processing and MHC class I-restricted cross-presentation by reducing disulfide bonds of endocy
101 oited by us to deliver viral epitopes, whose cross-presentation by the HLA-B27 molecules was proteaso
102 elopment or many primary infections requires cross-presentation by XCR1(+) dendritic cells (DCs).
103 y reveal that key steps of Ag processing for cross-presentation can be modulated by TLR ligands, open
109 er with adenovirus, a model for intrahepatic cross-presentation, confirms hepatocytes directly contri
110 rly demonstrate that CD8alpha(+) DC-mediated cross-presentation does not significantly contribute to
111 s I pathway; thus, it is widely assumed that cross-presentation drives the priming of antiviral T cel
114 o distinct endocytic compartments determines cross presentation efficiency, possibly by influencing a
115 , to analyze Sec61's contribution to antigen cross-presentation, ERAD, and transport of internalized
118 This selectivity does not extend to antigen cross-presentation for T-cell proliferation but is requi
120 h early and late endosomes appear to support cross presentation in human DCs, internalization efficie
123 the spatiotemporal orchestration of antigen cross-presentation in antigen-presenting cells with inna
124 of spatio-temporal orchestration of antigen cross-presentation in antigen-presenting cells with inna
126 is study demonstrates a mechanism regulating cross-presentation in cancer and suggests potential ther
130 enzyme that prepares antigenic epitopes for cross-presentation in dendritic cells, in complex with a
131 sion, strongly suggesting a role for in situ cross-presentation in local antigen-driven T(RM) differe
133 ammaR) antigen targeting facilitates antigen cross-presentation in several DC subsets, including BDCA
134 the micelles significantly enhanced antigen cross-presentation in vitro relative to free ovalbumin,
136 response by efficiently stimulating antigen cross-presentation in vivo and in vitro assessed by BMDC
142 In TAP-deficient mouse dendritic cells, cross-presentation is enhanced by the introduction of hu
147 leoprotein (NP)(366-374) presentation, while cross-presentation is optimal for acid polymerase (PA)(2
150 vitro activation, suggesting that in humans cross-presentation is restricted to certain DC subsets.
152 response can be generated in a system where cross-presentation is shut down by pretreatment with CpG
154 of IAV-specific CD8 T cells, suggesting that cross-presentation is sufficient for cytotoxic T lymphoc
155 8(+) T cell epitope frequently used to study cross-presentation, is ATP-dependent but substantially T
156 ression of genes encoding elements of the Ag cross-presentation machinery (i.e., of proteasome matura
158 upport a previously unrecognized model of Ag cross-presentation mediated by HLA-F and MHC-I open conf
160 ent HIV-1-derived Ags to CD8(+) T cells in a cross-presentation model, we investigated whether LCs we
161 aded onto MHC-I molecules, a process called "cross-presentation." Neither the actual contribution of
162 summary, our data suggest that TLR2-mediated cross-presentation occurs through the upregulation of Ra
163 As expected, BDCA3(+) DCs were superior at cross presentation of antigens delivered to late endosom
164 directly and quantitatively by comparing the cross presentation of identical antigens conjugated with
165 the FcR CD32 led to uptake, processing, and (cross-) presentation of encapsulated Ag to both CD4(+) a
166 eviously reported that the HLA-A2-restricted cross-presentation of a long peptide derived from melano
167 article, we show that the HLA-A1-restricted cross-presentation of a long peptide derived from tumor
168 ngle tumor released doxorubicin and enhanced cross-presentation of a model antigen at distant tumor s
169 ts with PEI/DNA complexes leads to efficient cross-presentation of a model antigen by dendritic cells
170 study shows that cDCs are indispensable for cross-presentation of ablation-released tumor antigens a
173 confirms hepatocytes directly contribute to cross-presentation of Ags and priming the pool of naive
177 cells in wild-type animals was dependent on cross-presentation of antigen by cells of the tumor stro
178 ficantly more efficient lysosomal escape and cross-presentation of antigen from dendritic cells (DCs)
179 ty peptide-MHC interactions led to efficient cross-presentation of antigen, thereby stimulating cogna
180 e and readily processed soluble proteins for cross-presentation of antigenic peptides to CD8(+) T cel
181 duce virus-specific CD8+ T cells through the cross-presentation of antigens from virally infected cel
182 Finally, consistent with their defect in the cross-presentation of apoptotic cells, DC-specific Vps34
184 t aged murine DCs were less efficient in the cross-presentation of cell-associated Ag and subsequentl
185 ying cells by CD8alpha(+) dendritic cells or cross-presentation of cell-associated Ag to CD8(+) T cel
189 causes the receptor to signal and potentiate cross-presentation of dead cell-associated antigens by D
190 actin exposed by dying cells and facilitates cross-presentation of dead cell-associated antigens by d
191 gand binding led to loss of DNGR-1-dependent cross-presentation of dead cell-associated antigens, for
192 cruits the tyrosine kinase Syk to promote DC cross-presentation of dead cell-associated antigens.
193 strength-dependent manner and that controls cross-presentation of dead cell-associated antigens.
194 41 is a negative regulator of Clec9A and the cross-presentation of dead cell-derived antigens by mous
195 om destructive to productive and facilitates cross-presentation of disease-relevant epitopes to CD8(+
197 vitro, increased HER2 uptake by DC increased cross-presentation of E75, the immunodominant epitope de
198 pression as well as antigenic stimulation by cross-presentation of EBV antigen from destroyed B cells
201 e for human pDCs as professional APCs in the cross-presentation of exogenous Ags is being re-evaluate
202 iated DCs, tumor-derived factors blocked the cross-presentation of exogenous Ags without inhibiting t
205 ptide to CD8(+) T cells occurs normally, but cross-presentation of GRP94/VSV8 complexes is defective.
207 pDC are capable of classical presentation or cross-presentation of IAV antigens and could potentially
208 genous tumor-reactive CD8(+) T cells via the cross-presentation of IgG complexed antigens (IgG IC), a
210 nd DCs failed to have a strong effect on the cross-presentation of immune complex (IC) OVA Ag to CD8(
213 e involvement of the vacuolar pathway in the cross-presentation of long peptides, and indicate that T
214 nal dendritic (cDC1) cells are necessary for cross-presentation of many viral and tumor antigens to C
215 uble antigen, suggesting that processing and cross-presentation of nano-particulate antigen is favore
217 atf3-dependent dendritic cells specialize in cross-presentation of necrotic tissue-derived epitopes t
219 C-I) presentation in dendritic cells enables cross-presentation of peptides derived from phagocytosed
221 e, the frequently reported TAP dependence of cross-presentation of phagocytosed OVA may principally r
222 n, including breast cancer, which results in cross-presentation of PR1, an NE-derived HLA-A2-restrict
224 eperfusion injury also promoted DC-dependent cross-presentation of renal antigens to CD8 T cells in t
228 n unrecognized tumor immune escape involving cross-presentation of systemically circulating tumor ant
229 as opposed to the HLA-A2-restricted peptide, cross-presentation of the HLA-A1-restricted peptide is T
230 c patients to MN-derived DCs (moDCs) induced cross-presentation of the intracellular reservoir of vir
232 s showed that NK cells inhibited DC-mediated cross-presentation of tumor Ags both in vivo and in vitr
233 s, stroma destruction, due to MHC-restricted cross-presentation of tumor antigens to T cells, may be
234 rs tumor cell autophagy and that it improves cross-presentation of tumor antigens to the immune syste
235 tment activated dendritic cells and enhanced cross-presentation of tumor-associated antigens to CD8 T
236 F1 in classical dendritic cells enhanced the cross-presentation of tumour antigens and the cross-prim
237 odies (Abs) that facilitated the capture and cross-presentation of viral Ags by FcgammaR-expressing D
239 non-redundant ability of DNGR-1 to regulate cross-presentation of viral antigens suggests that this
241 , Ags from immune complexes undergo enhanced cross-presentation on DC, leading to greater CD8 T cell
243 OX2, previously recognized to participate in cross-presentation, on phagosomes, thereby filling in a
244 ear whether this reflects specialization for cross presentation or a generally enhanced ability to pr
245 the proteasome- and TAP-dependent cytosolic cross-presentation pathway, previously shown to be used
246 Thus, we provide evidence for two separable cross-presentation pathways, only one of which is target
248 T cell survival: that rather than utilizing cross-presentation, pDC must be infected and utilize the
249 sults support a model in which host tumor Ag cross-presentation primes adoptively transferred T cells
255 cells) could offer the ideal environment for cross-presentation, resulting in cytotoxic immunity and
256 AB43 provides a specialized activity used in cross-presentation selectively by CD8alpha(+) DCs but no
258 DCs are not likely to possess mechanisms for cross presentation that are specific to this subset.
259 gand annexin1 is an important mediator in DC cross-presentation that increases efferocytosis in DCs a
260 we unravel a novel pathway of MHC I-mediated cross-presentation that is initiated with a host cellula
261 1 (cDC1) subpopulation important for antigen cross-presentation, that CD40L-overexpressing CAR T cell
265 Direct activation of DCs with PGN inhibited cross-presentation through nucleotide-binding oligomeriz
267 dendritic cells (DCs), and facilitate their cross presentation to stimulate an antitumor T-cell resp
268 ntation." Neither the actual contribution of cross-presentation to antitumor immune responses nor the
271 splenic CD8(+) DCs in vitro, namely antigen cross-presentation to CD8(+) T cells and secretion of IL
272 gonist treatment of mice inhibits Ag protein cross-presentation to CD8(+) T cells but preserves their
273 p-deficient dendritic cells induce increased cross-presentation to CD8(+) T cells by activating Rac2
277 ides locally generated by proteasomes allows cross-presentation to generate MHC-I-peptide complexes i
278 ude that the host uses mainly DCs capable of cross-presentation to induce the CMV-specific CD8(+) T c
280 alpha-DEC205, and alpha-Clec9A also mediated cross-presentation to primed CD8(+) T cells if, in paral
281 ellular pathways collectively referred to as cross-presentation to stimulate CD8(+) T cells with pept
282 40-48 epitope into productive processing and cross-presentation to strongly autoaggressive CTLs.
284 the class I-mediated antigen processing and cross-presentation transcriptional modules that were not
289 e cytosol, suggesting that the inhibition of cross-presentation was not related to either of these tr
293 ome-dependent class I MHC-restricted peptide cross-presentation when delivered by alphaDEC205 in vitr
295 lls (cDC1)(1) are thought to perform antigen cross-presentation, which is required to prime CD8(+) T
299 , which reactivate CTL by increasing antigen cross-presentation within the tumor microenvironment.