ライフサイエンスコーパス: cross-presentation

1 rnalization, CD40, was the most efficient at cross presentation.

2 n to MHC class I molecules, a process termed cross presentation.

3 role of oxidized lipids in the regulation of cross-presentation.

4 to elucidate the mechanisms of TLR2-mediated cross-presentation.

5 trols phagosomal pH, a critical parameter in cross-presentation.

6 --that mediates DC efferocytosis and antigen cross-presentation.

7 ulation of nonoxidized lipids did not affect cross-presentation.

8 ctive of T-cell receptor affinity or antigen cross-presentation.

9 ell immunity to these pathogens necessitates cross-presentation.

10 ate naive CD8(+) T cells in a process termed cross-presentation.

11 teasomal degradation products and blocked Ag cross-presentation.

12 mic reticulum-phagosome traffic required for cross-presentation.

13 ose of a less pure LPS preparation inhibited cross-presentation.

14 DCs are responsible for antigen exchange and cross-presentation.

15 to pure LPS abrogated its ability to enhance cross-presentation.

16 s of DC maturation on MHC class I-restricted cross-presentation.

17 strong as those induced exclusively through cross-presentation.

18 ose virus strains that are most dependent on cross-presentation.

19 class I loading in a process referred to as cross-presentation.

20 thereby optimizing XCR1(+) DC maturation and cross-presentation.

21 R)-mediated antigen uptake fails to initiate cross-presentation.

22 g DC immunoreceptor (DCIR) to mediate potent cross-presentation.

23 lpha(+) dendritic cells (DCs) in exosomal Ag cross-presentation.

24 gnition of such antigens by CD8+ T cells, or cross-presentation.

25 o draining lymph nodes, and enhances antigen cross-presentation.

26 te defects in both CD8 T cell activation and cross-presentation.

27 lar milieu on MHC-I through a process called cross-presentation.

28 I (MHC-I) molecules are the centerpieces of cross-presentation.

29 the two conformational states to potentiate cross-presentation.

30 ated C-type lectin receptors fail to promote cross-presentation.

31 f which contributes to the fine-tuning of Ag cross-presentation.

32 d mediates the power of DC efferocytosis and cross-presentation.

33 st be deployed to deliver Ag to pDCs for Ag (cross-)presentation.

34 ient (FcgammaR quadruple(-/-)) mice, and the cross-presentation ability of CD8alpha(+) DCs was not af

35 e investigated the mechanisms underlying the cross-presentation ability of IFN-DCs by studying the in

36 Cross-presentation allows antigen-presenting cells to pr

37 We used cross-presentation and CD137 activation-based FACS to en

38 toxicity is desirable and even necessary for cross-presentation and cross-priming of T cells.

39 Cross-presentation and crosspriming depend not only on T

40 ogel significantly enhanced antigen-specific cross-presentation and cytotoxic T lymphocyte (CTL) acti

41 ockade also potently suppressed both antigen cross-presentation and direct presentation of synthetic

42 organ-resident CD8(+) DCs are specialized at cross-presentation and have developed specific adaptatio

43 94 surface binding, endocytosis, and peptide cross-presentation and identify a role for heparin sulfa

44 of CD8alpha(+) DCs extends beyond a role in cross-presentation and includes a critical role for acti

45 eeks of T cell-replete syngeneic HSCT led to cross-presentation and increased survival of lymphoma-be

46 istinct pathway that operates within DCs for cross-presentation and is required for the activation of

47 stress/corticosterone on MHC class I (MHC I) cross-presentation and priming and show that stress/cort

48 are unique organ-resident APCs capable of Ag cross-presentation and subsequent tolerization of naive

49 TLR3 engagement in CD8(+) DCs promotes cross-presentation and the acquisition of effector funct

50 The enhanced antigen cross-presentation and the increased APC recruitment to

51 3(+) mDCs are presented by both MHC class I (cross-presentation) and MHC class II to antigen-specific

52 T-cell priming include direct presentation, cross-presentation, and cross-dressing.

53 cific T cells poorly, despite its long-lived cross-presentation, and T cells primed against the short

54 in TLR-induced dendritic cell activation and cross-presentation, and thus is vital in host defense.

55 or CD11c, BDCA1(+) DCs were as efficient at cross presentation as BDCA3(+) DCs.

56 Together, our data identify cross-presentation as a novel mechanism through which ce

57 tor (TLR) 7/8 agonist enhanced DCIR-mediated cross-presentation as well as cross-priming, particularl

58 riming and tumor rejection required tumor Ag cross-presentation, as evidenced by tumor outgrowth in K

59 wn as IFN-DCs, highly efficient in mediating cross-presentation, as well as the cross-priming of CD8(

60 This was probably due to promotion of cross-presentation because it was not detected when the

61 es IC uptake and is essentially required for cross-presentation, but not for MHC class II Ag presenta

62 en Ag presentation in vivo was restricted to cross-presentation, but the presence of T Ag-transformed

63 n vitro scavenging of ROS partially restored cross-presentation by aged DCs.

64 lysaccharide and interferon-gamma as well as cross-presentation by bone marrow-derived dendritic cell

65 Moreover, no detectable Ag cross-presentation by CD8alpha(+) DCs from C1qa(-/-) mic

66 In this study, to examine cross-presentation by classical dendritic cells (DCs; cD

67 TLR-stimulated cross-presentation by conventional dendritic cells (cDCs

68 cell responses were attributed to increased cross-presentation by DCs along with increased detection

69 Consequently, U-Omp19 enhances Ag cross-presentation by DCs to CD8(+) T cells.

70 The contribution of antigen cross-presentation by DCs to the induction of anti-viral

71 BBL resulted in increased antigen uptake and cross-presentation by DCs, leading to the generation of

72 educe IRAP-dependent but not ERAP1-dependent cross-presentation by dendritic cells with nanomolar eff

73 s and mediators, IgE-mediated tumour antigen cross-presentation by dendritic cells, as well as immuno

74 s that, through both direct presentation and cross-presentation by dendritic cells, purge the develop

75 3(+) DCs and not BDCA-1(+) DCs show improved cross-presentation by FcgammaR targeting, as measured by

76 Modulation of cross-presentation by Ig was inhibited by coapplication

77 sociated with a marked inhibition in antigen cross-presentation by Igfbp7(-/-) dendritic cells.

78 ontrast to classical spleen dendritic cells, cross-presentation by liver antigen-presenting cells was

79 Antigen cross-presentation by liver cells induced efficient CD8+

80 f HA-1 long peptide resulted in efficient Ag cross-presentation by mDCs and pDCs, leading to strong e

81 ning the tyrosine signal but does not affect cross-presentation by MHC-I containing the HLA-C cytopla

82 In APCs, we show that HIV Nef disrupts cross-presentation by MHC-I containing the tyrosine sign

83 in adaptor protein 1 (AP-1) is necessary for cross-presentation by MHC-I molecules containing a cytop

84 n contrast, AP-1 activity was not needed for cross-presentation by MHC-I molecules containing a human

85 We also studied LP cross-presentation by monocyte-derived DC, plasmacytoid

86 modified LP gave rise to high and sustained cross-presentation by monocyte-derived DC.

87 ntigen processing and MHC class I-restricted cross-presentation by reducing disulfide bonds of endocy

88 Oxidized lipids blocked cross-presentation by reducing the expression of peptide

89 Surprisingly, antigen cross-presentation by resident CX3CR1(+) DCs induced dif

90 oited by us to deliver viral epitopes, whose cross-presentation by the HLA-B27 molecules was proteaso

91 elopment or many primary infections requires cross-presentation by XCR1(+) dendritic cells (DCs).

92 y reveal that key steps of Ag processing for cross-presentation can be modulated by TLR ligands, open

93 Mouse XCR1(+) DC excel at cross-presentation, can be targeted in vivo to induce pr

94 The robust cross-presentation capability appears to be a hallmark o

95 C class I exogenous peptide presentation and cross-presentation capacities.

96 Taken together, their cross-presentation capacity and type I IFN production to

97 Despite dampened cross-presentation capacity, batf3(-/-) chimeras had equ

98 but not macrophages, display high intrinsic cross-presentation capacity.

99 er with adenovirus, a model for intrahepatic cross-presentation, confirms hepatocytes directly contri

100 rly demonstrate that CD8alpha(+) DC-mediated cross-presentation does not significantly contribute to

101 s I pathway; thus, it is widely assumed that cross-presentation drives the priming of antiviral T cel

102 somes with ERC-derived MHC-I, and subsequent cross-presentation during infection.

103 taining vesicles contributes to the superior cross-presentation efficacy of CD8(+) cDCs.

104 o distinct endocytic compartments determines cross presentation efficiency, possibly by influencing a

105 , to analyze Sec61's contribution to antigen cross-presentation, ERAD, and transport of internalized

106 DCs from these mice show impaired cross-presentation ex vivo and defective cross-priming o

107 Thus, the requirement of IRAP in cross-presentation extends to steady-state cDCs.

108 endent for NY-ESO-1(60-72)/HLA-B7-restricted cross-presentation facilitated by ISCOMATRIX adjuvant.

109 This selectivity does not extend to antigen cross-presentation for T-cell proliferation but is requi

110 The study of cross-presentation has been focused on the relative cont

111 t endocytosis pathway in APCs and facilitate cross presentation in a highly regulated manner.

112 h early and late endosomes appear to support cross presentation in human DCs, internalization efficie

113 Pretreatment with pure LPS increased cross-presentation in a manner dependent on both MyD88 a

114 V mutants to elucidate the pathway of capsid cross-presentation in AAV-permissive cells.

115 the spatiotemporal orchestration of antigen cross-presentation in antigen-presenting cells with inna

116 of spatio-temporal orchestration of antigen cross-presentation in antigen-presenting cells with inna

117 s a NE receptor that mediates uptake and PR1 cross-presentation in breast cancer cells.

118 is study demonstrates a mechanism regulating cross-presentation in cancer and suggests potential ther

119 These studies thus demonstrate that cross-presentation in CD8(-)CD11b(+) DCs requires a two-

120 We find that impaired cross-presentation in DCs is largely associated with def

121 We conclude that Sec22b-dependent cross-presentation in DCs is required to initiate CD8(+)

122 Although antigen cross-presentation in dendritic cells (DCs) is critical

123 enzyme that prepares antigenic epitopes for cross-presentation in dendritic cells, in complex with a

124 1 substrates is the cause of altered antigen cross-presentation in Sec61-blocked DCs.

125 ammaR) antigen targeting facilitates antigen cross-presentation in several DC subsets, including BDCA

126 the micelles significantly enhanced antigen cross-presentation in vitro relative to free ovalbumin,

127 ound that both combinations promoted antigen cross-presentation in vitro.

128 response by efficiently stimulating antigen cross-presentation in vivo and in vitro assessed by BMDC

129 dicating that Sec61 blockade affects antigen cross-presentation indirectly.

130 Ag cross presentation is an important mechanism for CD8(+)

131 Cross-presentation is a critical function of dendritic c

132 Cross-presentation is a key function of dendritic cells

133 Cross-presentation is a modular series of intracellular

134 Antigen cross-presentation is a principal function of specialize

135 Cross-presentation is considered the primary mode of ant

136 FcRn-driven cross-presentation is further shown to control cross-pri

137 Dendritic cell (DC) Ag cross-presentation is generally associated with immune r

138 Antiviral immunity and cross-presentation is mediated constitutively through CD

139 Moreover, inhibition of cross-presentation is neither due to reduced costimulato

140 Cross-presentation is one of the main features of dendri

141 ly contaminant responsible for shutting down cross-presentation is peptidoglycan (PGN).

142 vitro activation, suggesting that in humans cross-presentation is restricted to certain DC subsets.

143 We further showed that LP cross-presentation is restricted to monocytes and conven

144 response can be generated in a system where cross-presentation is shut down by pretreatment with CpG

145 However, how TLR triggering can affect Ag cross-presentation is still not clear.

146 of IAV-specific CD8 T cells, suggesting that cross-presentation is sufficient for cytotoxic T lymphoc

147 8(+) T cell epitope frequently used to study cross-presentation, is ATP-dependent but substantially T

148 ression of genes encoding elements of the Ag cross-presentation machinery (i.e., of proteasome matura

149 f key components of the phagosome-to-cytosol cross-presentation machinery.

150 related markers on B cells and activated the cross-presentation machinery.

151 upport a previously unrecognized model of Ag cross-presentation mediated by HLA-F and MHC-I open conf

152 This increased E75 cross-presentation, mediated by trastuzumab treatment, e

153 ent HIV-1-derived Ags to CD8(+) T cells in a cross-presentation model, we investigated whether LCs we

154 aded onto MHC-I molecules, a process called "cross-presentation." Neither the actual contribution of

155 summary, our data suggest that TLR2-mediated cross-presentation occurs through the upregulation of Ra

156 As expected, BDCA3(+) DCs were superior at cross presentation of antigens delivered to late endosom

157 Cross presentation of Hsp90-chaperoned peptides through

158 directly and quantitatively by comparing the cross presentation of identical antigens conjugated with

159 shock protein 90 (Hsp90) chaperone-mediated cross presentation of OVA-derived Ags.

160 the FcR CD32 led to uptake, processing, and (cross-) presentation of encapsulated Ag to both CD4(+) a

161 GILT is essential for cross-presentation of a CD8+ T cell epitope of glycoprot

162 ate the indirect presentation as well as the cross-presentation of a larger repertoire of "linked" do

163 ts with PEI/DNA complexes leads to efficient cross-presentation of a model antigen by dendritic cells

164 study shows that cDCs are indispensable for cross-presentation of ablation-released tumor antigens a

165 , persistence of virally infected cells, and cross-presentation of Ag.

166 confirms hepatocytes directly contribute to cross-presentation of Ags and priming the pool of naive

167 They altered cross-presentation of Ags by dendritic cells to epitope-

168 Cross-presentation of Ags by osteoclasts leads to expres

169 An apparent cross-presentation of antigen acquired from muscle sugge

170 cells in wild-type animals was dependent on cross-presentation of antigen by cells of the tumor stro

171 ficantly more efficient lysosomal escape and cross-presentation of antigen from dendritic cells (DCs)

172 ty peptide-MHC interactions led to efficient cross-presentation of antigen, thereby stimulating cogna

173 e and readily processed soluble proteins for cross-presentation of antigenic peptides to CD8(+) T cel

174 dritic cells (DCs) are important in vivo for cross-presentation of antigens derived from intracellula

175 duce virus-specific CD8+ T cells through the cross-presentation of antigens from virally infected cel

176 Finally, consistent with their defect in the cross-presentation of apoptotic cells, DC-specific Vps34

177 We investigate the mechanisms of cross-presentation of associated peptides and co-stimula

178 t aged murine DCs were less efficient in the cross-presentation of cell-associated Ag and subsequentl

179 ying cells by CD8alpha(+) dendritic cells or cross-presentation of cell-associated Ag to CD8(+) T cel

180 ent monocyte-derived DCs showed no defect in cross-presentation of cell-associated antigen.

181 s but show a defect for in vivo and in vitro cross-presentation of cell-associated antigen.

182 gest that DNGR-1 is a dedicated receptor for cross-presentation of cell-associated antigens.

183 causes the receptor to signal and potentiate cross-presentation of dead cell-associated antigens by D

184 actin exposed by dying cells and facilitates cross-presentation of dead cell-associated antigens by d

185 gand binding led to loss of DNGR-1-dependent cross-presentation of dead cell-associated antigens, for

186 strength-dependent manner and that controls cross-presentation of dead cell-associated antigens.

187 cruits the tyrosine kinase Syk to promote DC cross-presentation of dead cell-associated antigens.

188 om destructive to productive and facilitates cross-presentation of disease-relevant epitopes to CD8(+

189 Efficient cross-presentation of disulfide-rich antigens requires a

190 DNGR-1 was essential for cross-presentation of dying vaccinia virus-infected (VAC

191 vitro, increased HER2 uptake by DC increased cross-presentation of E75, the immunodominant epitope de

192 pression as well as antigenic stimulation by cross-presentation of EBV antigen from destroyed B cells

193 ss-priming of CD8(+) T cells, which requires cross-presentation of exogenous Ag to DCs.

194 The effects of TLR triggering on the cross-presentation of exogenous Ags by DCs remain unclea

195 e for human pDCs as professional APCs in the cross-presentation of exogenous Ags is being re-evaluate

196 iated DCs, tumor-derived factors blocked the cross-presentation of exogenous Ags without inhibiting t

197 Activation markers, cross-presentation of exogenous Ags, and activation of C

198 Dendritic cell (DC)-mediated cross-presentation of exogenous antigens acquired in the

199 Anti-hDEC205 also improved the cross-presentation of Gag to primed CD8(+) T cells from

200 The role of CD91 in the cross-presentation of GRP94-associated peptides was exam

201 ptide to CD8(+) T cells occurs normally, but cross-presentation of GRP94/VSV8 complexes is defective.

202 t time, proteasome-dependent and independent cross-presentation of HLA-A-, B-, and C-restricted epito

203 Following cross-presentation of HSP-chaperoned peptides by CD91(+)

204 pDC are capable of classical presentation or cross-presentation of IAV antigens and could potentially

205 genous tumor-reactive CD8(+) T cells via the cross-presentation of IgG complexed antigens (IgG IC), a

206 onatal Fc receptor for IgG (FcRn) to conduct cross-presentation of IgG ICs.

207 Cross-presentation of IgG-containing immune complexes (I

208 nd DCs failed to have a strong effect on the cross-presentation of immune complex (IC) OVA Ag to CD8(

209 ) efficiently facilitate the presentation or cross-presentation of immune-complexed Ags to T cells.

210 B-cell cross-presentation of insulin required proteolytic cleav

211 tic cells responsible for mediating both the cross-presentation of islet Ags to CD8(+) T cells and th

212 In this study, we show cross-presentation of islet-derived autoantigens by B ce

213 only inhibited apoptosis but also prevented cross-presentation of its antigens by dendritic cells, w

214 uble antigen, suggesting that processing and cross-presentation of nano-particulate antigen is favore

215 While cross-presentation of native OVA requires high antigen d

216 atf3-dependent dendritic cells specialize in cross-presentation of necrotic tissue-derived epitopes t

217 Finally, cross-presentation of NY-ESO-1(157-165)/HLA-A2, NY-ESO-1

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 In contrast, cross-presentation of peptides on MHC I was intact in th

221 Cross-presentation of phagocytosed Ags by MHC class I (M

222 e, the frequently reported TAP dependence of cross-presentation of phagocytosed OVA may principally r

223 n, including breast cancer, which results in cross-presentation of PR1, an NE-derived HLA-A2-restrict

224 Efficient cross-presentation of protein Ags to CTLs by dendritic c

225 Cs are as active as classical DCs, including cross-presentation of proteins and live gram-negative ba

226 eperfusion injury also promoted DC-dependent cross-presentation of renal antigens to CD8 T cells in t

227 IRAP deficiency compromised cross-presentation of soluble and particulate Ag by both

228 immunoglobulins (Ig) in vivo are impaired in cross-presentation of soluble antigen.

229 eral Ags to LECs, which maintain tolerogenic cross-presentation of such Ags.

230 n unrecognized tumor immune escape involving cross-presentation of systemically circulating tumor ant

231 We studied cross-presentation of the cancer/testis antigen, NY-ESO-

232 CD91 on antigen-presenting cells (APCs) for cross-presentation of the HSP-chaperoned peptides.

233 c patients to MN-derived DCs (moDCs) induced cross-presentation of the intracellular reservoir of vir

234 The uptake and long-term cross-presentation of tumor Ag long peptides (LP) by den

235 s showed that NK cells inhibited DC-mediated cross-presentation of tumor Ags both in vivo and in vitr

236 s, stroma destruction, due to MHC-restricted cross-presentation of tumor antigens to T cells, may be

237 rs tumor cell autophagy and that it improves cross-presentation of tumor antigens to the immune syste

238 tment activated dendritic cells and enhanced cross-presentation of tumor-associated antigens to CD8 T

239 odies (Abs) that facilitated the capture and cross-presentation of viral Ags by FcgammaR-expressing D

240 cells are effectively primed against CPXV by cross-presentation of viral Ags in young mice.

241 non-redundant ability of DNGR-1 to regulate cross-presentation of viral antigens suggests that this

242 ear whether this reflects specialization for cross presentation or a generally enhanced ability to pr

243 ssing via the cytosolic proteasome-dependent cross-presentation pathway.

244 Thus, we provide evidence for two separable cross-presentation pathways, only one of which is target

245 iated with Ag processing-dependent auxiliary cross-presentation pathways.

246 ence and uptake, but on the engagement of DC cross-presentation pathways.

247 T cell survival: that rather than utilizing cross-presentation, pDC must be infected and utilize the

248 sults support a model in which host tumor Ag cross-presentation primes adoptively transferred T cells

249 These deficits in cross-presentation/priming were not due to altered Ag do

250 4(+)CD8alpha(+) DC subset, which carries out cross-presentation/priming, was preferentially depleted

251 reas ROS interfered with a later step in the cross-presentation process.

252 The mechanisms of cross presentation remain incompletely understood, parti

253 We further show that PR1 cross-presentation renders human breast cancer and melan

254 FcgammaR-facilitated cross-presentation requires antigen processing in both a

255 Although cross-presentation requires Sec22b-mediated phagosomal r

256 cells) could offer the ideal environment for cross-presentation, resulting in cytotoxic immunity and

257 AB43 provides a specialized activity used in cross-presentation selectively by CD8alpha(+) DCs but no

258 Collectrin-mediated cross-presentation supports intrahepatic adaptive antivi

259 DCs are not likely to possess mechanisms for cross presentation that are specific to this subset.

260 gand annexin1 is an important mediator in DC cross-presentation that increases efferocytosis in DCs a

261 we unravel a novel pathway of MHC I-mediated cross-presentation that is initiated with a host cellula

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 mechanisms underlying MHC class I-restricted cross-presentation, the transfer of Ag from an infected

265 Given the centrality of FcRn in controlling cross-presentation, these studies lay the foundation for

266 Direct activation of DCs with PGN inhibited cross-presentation through nucleotide-binding oligomeriz

267 ntation." Neither the actual contribution of cross-presentation to antitumor immune responses nor the

268 This facilitates its cross-presentation to autoaggressive cytotoxic MHC-E-res

269 to CD4 T cells but impacts the efficiency of cross-presentation to CD8 T cells.

270 splenic CD8(+) DCs in vitro, namely antigen cross-presentation to CD8(+) T cells and secretion of IL

271 gonist treatment of mice inhibits Ag protein cross-presentation to CD8(+) T cells but preserves their

272 p-deficient dendritic cells induce increased cross-presentation to CD8(+) T cells by activating Rac2

273 proteins similarly activated CD4(+) T cells, cross-presentation to CD8(+) T cells was only efficientl

274 a recycling endosomal compartment, favoring cross-presentation to CD8(+) T cells.

275 s from these mice display defects in antigen cross-presentation to CD8(+) T cells.

276 ve increased activation of Rac2 that support cross-presentation to CD8(+) T cells.

277 both through MHC class II expression and in cross-presentation to CD8s.

278 This unique mechanism thus enables cross-presentation to evolve from an atypically acidic l

279 ude that the host uses mainly DCs capable of cross-presentation to induce the CMV-specific CD8(+) T c

280 f IgG ICs to the proper destination for such cross-presentation to occur.

281 alpha-DEC205, and alpha-Clec9A also mediated cross-presentation to primed CD8(+) T cells if, in paral

282 ellular pathways collectively referred to as cross-presentation to stimulate CD8(+) T cells with pept

283 40-48 epitope into productive processing and cross-presentation to strongly autoaggressive CTLs.

284 , as well as reduced immune complex-mediated cross-presentation to T cells.

285 olving recombinant technology and class I Ag cross-presentation, to search for supraoptimal superagon

286 the class I-mediated antigen processing and cross-presentation transcriptional modules that were not

287 t nucleated cells and exogenous proteins for cross-presentation typically by professional APCs.

288 Cross-presentation using splenic NOTAM DCs and prolonged

289 via alternative means, potentially including cross-presentation via the MHC class II pathway.

290 The decreased cross-presentation was associated with a reduction in th

291 cells, which express CD91, GRP94.NTD-peptide cross-presentation was insensitive to the CD91 ligands r

292 e cytosol, suggesting that the inhibition of cross-presentation was not related to either of these tr

293 This cross-presentation was sensitive to inhibitors of lysoso

294 Apparently, this cross-presentation was TAP-independent, as it was conduc

295 To investigate how STAT2 affects cross-presentation, we determined its requirements for d

296 To study cross-presentation, we used hosts that express defined M

297 ome-dependent class I MHC-restricted peptide cross-presentation when delivered by alphaDEC205 in vitr

298 The observed enhancement in OVA cross-presentation with polyU in DCs could be mediated b

299 In contrast, both classic and cross-presentation within MHC class I remain largely int

300 , which reactivate CTL by increasing antigen cross-presentation within the tumor microenvironment.