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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
45                                              Cross-presentation allows antigen-presenting cells to pr
46                                              Cross-presentation allows dendritic cells (DCs) to prese
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.
50                                      We used cross-presentation and CD137 activation-based FACS to en
51 ype 1 dendritic cells that are essential for cross-presentation and CD8 T cell-mediated immunity agai
52 toxicity is desirable and even necessary for cross-presentation and cross-priming of T cells.
53 bulk large tumors, release tumor antigen for cross-presentation and cross-priming, release cancer-sup
54                                              Cross-presentation and crosspriming depend not only on T
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
63       TLR3 engagement in CD8(+) DCs promotes cross-presentation and the acquisition of effector funct
64                         The enhanced antigen cross-presentation and the increased APC recruitment to
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
67  T-cell priming include direct presentation, cross-presentation, and cross-dressing.
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.
70  or CD11c, BDCA1(+) DCs were as efficient at cross presentation as BDCA3(+) DCs.
71                  Together, our data identify cross-presentation as a novel mechanism through which ce
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(
74        This was probably due to promotion of cross-presentation because it was not detected when the
75 es IC uptake and is essentially required for cross-presentation, but not for MHC class II Ag presenta
76 n vitro scavenging of ROS partially restored cross-presentation by aged DCs.
77 lysaccharide and interferon-gamma as well as cross-presentation by bone marrow-derived dendritic cell
78                   Moreover, no detectable Ag cross-presentation by CD8alpha(+) DCs from C1qa(-/-) mic
79                    In this study, to examine cross-presentation by classical dendritic cells (DCs; cD
80                               TLR-stimulated cross-presentation by conventional dendritic cells (cDCs
81  cell responses were attributed to increased cross-presentation by DCs along with increased detection
82            Consequently, U-Omp19 enhances Ag cross-presentation by DCs to CD8(+) T cells.
83                  The contribution of antigen cross-presentation by DCs to the induction of anti-viral
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
88                                Modulation of cross-presentation by Ig was inhibited by coapplication
89 sociated with a marked inhibition in antigen cross-presentation by Igfbp7(-/-) dendritic cells.
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
93       In APCs, we show that HIV Nef disrupts cross-presentation by MHC-I containing the tyrosine sign
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
96                           We also studied LP cross-presentation by monocyte-derived DC, plasmacytoid
97  modified LP gave rise to high and sustained cross-presentation by monocyte-derived DC.
98 ntigen processing and MHC class I-restricted cross-presentation by reducing disulfide bonds of endocy
99                      Oxidized lipids blocked cross-presentation by reducing the expression of peptide
100                        Surprisingly, antigen cross-presentation by resident CX3CR1(+) DCs induced dif
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
104                    Mouse XCR1(+) DC excel at cross-presentation, can be targeted in vivo to induce pr
105 C class I exogenous peptide presentation and cross-presentation capacities.
106                        Taken together, their cross-presentation capacity and type I IFN production to
107                             Despite dampened cross-presentation capacity, batf3(-/-) chimeras had equ
108  but not macrophages, display high intrinsic cross-presentation capacity.
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
112 somes with ERC-derived MHC-I, and subsequent cross-presentation during infection.
113 taining vesicles contributes to the superior cross-presentation efficacy of CD8(+) cDCs.
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
116            DCs from these mice show impaired cross-presentation ex vivo and defective cross-priming o
117             Thus, the requirement of IRAP in cross-presentation extends to steady-state cDCs.
118  This selectivity does not extend to antigen cross-presentation for T-cell proliferation but is requi
119                                 The study of cross-presentation has been focused on the relative cont
120 h early and late endosomes appear to support cross presentation in human DCs, internalization efficie
121         Pretreatment with pure LPS increased cross-presentation in a manner dependent on both MyD88 a
122 V mutants to elucidate the pathway of capsid cross-presentation in AAV-permissive cells.
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
125 s a NE receptor that mediates uptake and PR1 cross-presentation in breast cancer cells.
126 is study demonstrates a mechanism regulating cross-presentation in cancer and suggests potential ther
127                        We find that impaired cross-presentation in DCs is largely associated with def
128            We conclude that Sec22b-dependent cross-presentation in DCs is required to initiate CD8(+)
129                             Although antigen cross-presentation in dendritic cells (DCs) is critical
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
132 1 substrates is the cause of altered antigen cross-presentation in Sec61-blocked DCs.
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,
135 ound that both combinations promoted antigen cross-presentation in vitro.
136  response by efficiently stimulating antigen cross-presentation in vivo and in vitro assessed by BMDC
137 dicating that Sec61 blockade affects antigen cross-presentation indirectly.
138                                              Cross-presentation is a critical function of dendritic c
139                                              Cross-presentation is a key function of dendritic cells
140                                              Cross-presentation is a modular series of intracellular
141                                              Cross-presentation is considered the primary mode of ant
142      In TAP-deficient mouse dendritic cells, cross-presentation is enhanced by the introduction of hu
143                       Dendritic cell (DC) Ag cross-presentation is generally associated with immune r
144                       Antiviral immunity and cross-presentation is mediated constitutively through CD
145                      Moreover, inhibition of cross-presentation is neither due to reduced costimulato
146                                              Cross-presentation is one of the main features of dendri
147 leoprotein (NP)(366-374) presentation, while cross-presentation is optimal for acid polymerase (PA)(2
148                                              Cross-presentation is particularly effective with long s
149 ly contaminant responsible for shutting down cross-presentation is peptidoglycan (PGN).
150  vitro activation, suggesting that in humans cross-presentation is restricted to certain DC subsets.
151                    We further showed that LP cross-presentation is restricted to monocytes and conven
152  response can be generated in a system where cross-presentation is shut down by pretreatment with CpG
153    However, how TLR triggering can affect Ag cross-presentation is still not clear.
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
157 related markers on B cells and activated the cross-presentation machinery.
158 upport a previously unrecognized model of Ag cross-presentation mediated by HLA-F and MHC-I open conf
159                           This increased E75 cross-presentation, mediated by trastuzumab treatment, e
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
171 , persistence of virally infected cells, and cross-presentation of Ag.
172 dosomal/lysosomal compartments necessary for cross-presentation of Ag.
173  confirms hepatocytes directly contribute to cross-presentation of Ags and priming the pool of naive
174                                 They altered cross-presentation of Ags by dendritic cells to epitope-
175                                              Cross-presentation of Ags by osteoclasts leads to expres
176                                  An apparent cross-presentation of antigen acquired from muscle sugge
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
183             We investigate the mechanisms of cross-presentation of associated peptides and co-stimula
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
186 ent monocyte-derived DCs showed no defect in cross-presentation of cell-associated antigen.
187 s but show a defect for in vivo and in vitro cross-presentation of cell-associated antigen.
188 gest that DNGR-1 is a dedicated receptor for cross-presentation of cell-associated antigens.
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(+
196                     DNGR-1 was essential for cross-presentation of dying vaccinia virus-infected (VAC
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
199 ss-priming of CD8(+) T cells, which requires cross-presentation of exogenous Ag to DCs.
200         The effects of TLR triggering on the cross-presentation of exogenous Ags by DCs remain unclea
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
203                          Activation markers, cross-presentation of exogenous Ags, and activation of C
204                 Dendritic cell (DC)-mediated cross-presentation of exogenous antigens acquired in the
205 ptide to CD8(+) T cells occurs normally, but cross-presentation of GRP94/VSV8 complexes is defective.
206                                    Following cross-presentation of HSP-chaperoned peptides by CD91(+)
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
209                                              Cross-presentation of IgG-containing immune complexes (I
210 nd DCs failed to have a strong effect on the cross-presentation of immune complex (IC) OVA Ag to CD8(
211                                       B-cell cross-presentation of insulin required proteolytic cleav
212                       In this study, we show cross-presentation of islet-derived autoantigens by B ce
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
216                                        While cross-presentation of native OVA requires high antigen d
217 atf3-dependent dendritic cells specialize in cross-presentation of necrotic tissue-derived epitopes t
218                      Moreover, MGL1-mediated cross-presentation of OVA-Le(X) neither required TAP-tra
219 C-I) presentation in dendritic cells enables cross-presentation of peptides derived from phagocytosed
220                                              Cross-presentation of phagocytosed Ags by MHC class I (M
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
223                                    Efficient cross-presentation of protein Ags to CTLs by dendritic c
224 eperfusion injury also promoted DC-dependent cross-presentation of renal antigens to CD8 T cells in t
225                  IRAP deficiency compromised cross-presentation of soluble and particulate Ag by both
226 immunoglobulins (Ig) in vivo are impaired in cross-presentation of soluble antigen.
227 eral Ags to LECs, which maintain tolerogenic cross-presentation of such Ags.
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
231                     The uptake and long-term cross-presentation of tumor Ag long peptides (LP) by den
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
238 cells are effectively primed against CPXV by cross-presentation of viral Ags in young mice.
239  non-redundant ability of DNGR-1 to regulate cross-presentation of viral antigens suggests that this
240 d inhibition of cathepsins markedly enhances cross-presentation of wild-type dendritic cells.
241 , Ags from immune complexes undergo enhanced cross-presentation on DC, leading to greater CD8 T cell
242 ntly acquires secreted mTEC-derived TRAs for cross-presentation on MHC-I.
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
247 iated with Ag processing-dependent auxiliary cross-presentation pathways.
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
250 reas ROS interfered with a later step in the cross-presentation process.
251                            The mechanisms of cross presentation remain incompletely understood, parti
252                     We further show that PR1 cross-presentation renders human breast cancer and melan
253                         FcgammaR-facilitated cross-presentation requires antigen processing in both a
254                                     Although cross-presentation requires Sec22b-mediated phagosomal r
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
257                          Collectrin-mediated cross-presentation supports intrahepatic adaptive antivi
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
262 pressed on the subset of DCs responsible for cross-presentation, the CD8(+) murine splenic DCs.
263                                           Ag cross-presentation, the process by which pathogen Ags ar
264                             Due to increased cross-presentation, these capped nanofibers trigger stro
265  Direct activation of DCs with PGN inhibited cross-presentation through nucleotide-binding oligomeriz
266            This synergy was dependent on TAA cross presentation to cytolytic CD8+ T cells and on IFN-
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
269                         This facilitates its cross-presentation to autoaggressive cytotoxic MHC-E-res
270 to CD4 T cells but impacts the efficiency of cross-presentation to CD8 T cells.
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
274 ve increased activation of Rac2 that support cross-presentation to CD8(+) T cells.
275  a recycling endosomal compartment, favoring cross-presentation to CD8(+) T cells.
276  both through MHC class II expression and in cross-presentation to CD8s.
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
279 f IgG ICs to the proper destination for such cross-presentation to occur.
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.
283 , as well as reduced immune complex-mediated cross-presentation to T cells.
284  the class I-mediated antigen processing and cross-presentation transcriptional modules that were not
285 t nucleated cells and exogenous proteins for cross-presentation typically by professional APCs.
286                                              Cross-presentation using splenic NOTAM DCs and prolonged
287 via alternative means, potentially including cross-presentation via the MHC class II pathway.
288                                The decreased cross-presentation was associated with a reduction in th
289 e cytosol, suggesting that the inhibition of cross-presentation was not related to either of these tr
290                                         This cross-presentation was sensitive to inhibitors of lysoso
291                             Apparently, this cross-presentation was TAP-independent, as it was conduc
292             To investigate how STAT2 affects cross-presentation, we determined its requirements for d
293 ome-dependent class I MHC-restricted peptide cross-presentation when delivered by alphaDEC205 in vitr
294                 The intracellular pathway of cross-presentation, which allows MHC class I-restricted
295 lls (cDC1)(1) are thought to perform antigen cross-presentation, which is required to prime CD8(+) T
296                  TNF stimulation augments LC cross-presentation while attenuating IRF4 expression.
297              The observed enhancement in OVA cross-presentation with polyU in DCs could be mediated b
298                In contrast, both classic and cross-presentation within MHC class I remain largely int
299 , which reactivate CTL by increasing antigen cross-presentation within the tumor microenvironment.
300 ccomplished through a pathway called antigen cross-presentation (XPT).

 
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