Key preclinical studies demonstrating dependence on cDC1 for successful immunotherapy
| Immunotherapy approach | Genetic model utilized | Tumor model utilized | Key findings | Reference |
|---|---|---|---|---|
| ICB | ||||
| αCXCR4 + αPD-1 IgG combination | Batf3−/− C57BL/6J | Orthotopic (HCA-1) and autochthonous HCC models | cDC1 prevalence and proximity to CD8+ T cells increased following combination therapy. Combination therapy effectiveness was compromised in KO mice | Morita et al. (2025) |
| αPD-L1 IgG | Chimeric mice: BM from CD11c-DTR-eGFP mice mixed with WT or Batf3−/− mice | B16-SIY and MC8-SIY SC models | Presence of cDC1s in the TME expressing the costimulatory molecule 4-1BBL required for optimal response to anti-PD-1 blockade | Ziblat et al. (2024) |
| αPD-1 + α4-1BB IgG combination | C57BL/6 XCR1DTRVenus B6.129S(C)-Batf3tm1Kmm/J | MC38 SC model | cDC1 depletion impaired therapeutic efficacy associated with reduced intratumoral T cell infiltration | Teijeira et al. (2022) |
| αPD-1 + αCTLA4 IgG alone and in combination | C57BL/6 Xcr1DTRVenus | E0771 SC model | cDC1 depletion impaired therapeutic efficacy | Teijeira et al. (2022) |
| αCTLA4 IgG | Batf3−/− C57BL/6 Xcr1DTRVenus | Orthotopic MOSC1 tongue tumor model | αCTLA4-targeted therapy resulted in increase of cDC1s in tdLN. Therapeutic response was diminished in Batf3−/− mice Early depletion of cDC1s relative to treatment impairs response, while later depletion had less impairment on therapeutic efficacy | Saddawi-Konefka et al. (2022) |
| αPD-1 IgG + CCL7 combination | N/A | Autochthonous KrasLSL−G12D/+Tp53fl/fl (KP) and the KrasLSL−G12D/+Lkb1fl/fl (KL) NSCLC mouse models | Combined treatment prolonged survival of mice compared with untreated and PD-1 treatment alone. Therapeutic efficacy was associated with increased infiltration of cDC1s and CD8+ T cells | Zhang et al. (2020) |
| αPD-L1 IgG | CD11c-Cre; Pdl1^fl/f and Batf3−/− C57BL/6J | MC38 and EG.7 SC models | PD-L1 expression on DCs essential for response to αPD-L1–targeted therapy. Efficacy of αPD-L1–targeted therapy was diminished in Batf3−/−mice. cDC1s upregulate PD-L1 upon antigen uptake driven by IFNγ signaling | Peng et al. (2020) |
| - | Clec9a-Cre Cd274fl/fl C57BL/6N mice (not cDC1 specific—all mature DCs) | PD-L1–deficient and PD-L1–sufficient MC38, and HEPA1-6.X1.1 SC models | Deletion of PD-L1 expression on DCs, and not macrophages, leads to restriction of tumor growth and enhanced antitumor T cell responses. DCs identified as key mediators of PD-1:PD-L1 axis | Oh et al. (2020) |
| αPD-1 + α4-1BB IgG | Batf3−/− BALB/C | Orthotopic 4T1.2 mammary carcinoma model | Adjuvant or neoadjuvant immunotherapy efficacy was diminished in Batf3−/− mice associated with reduced CD8+ T cell priming | Liu et al. (2019) |
| αPD-1 IgG | Zbtb46-Dtr chimera models | MC38 SC model | Efficacy of αPD-1–targeted therapy was impaired when DCs were depleted or when IL-12 was neutralized. Authors demonstrate a role for IL-12+ cDC1s for optimal therapeutic response | Garris et al. (2018) |
| αPD-L1 IgG | Batf3−/− C57BL/6J | B16 SC models | Efficacy of αPD-L1–targeted therapy was diminished in Batf3−/−mice. CD103+ DCs were required to induce treatment-induced antitumor immunity. Therapeutic synergy was observed between systemic FLT3L, αPD-L1 IgG, and intratumoral poly I:C treatment | Salmon et al. (2016) |
| αPD-1 + α4-1BB IgG alone and in combination α4-1BB IgG + IL-12 αPD-1 or α4-1BB IgG in combination with FLT3L and poly-ICLC | Batf3−/− C57BL/6J | MC38, MC38-OVA, and B16-OVA SC models | Efficacy of each immunotherapeutic approach trialed was diminished in Batf3−/− mice associated with the absence of CD8+ T cell priming | Sánchez-Paulete et al. (2016) |
| Costimulatory agonist therapy | ||||
| Systemic α4-1BB IgG in combination with intratumoral HMGN1 (TLR4 agonist) and 3M-052 (TLR7/8 agonist) ISV | Batf3−/− C57BL/6J | MC38 SC models | Combination therapy efficacy was diminished in Batf3−/− mice associated with lower secretion of IFNγ by T cells in treated mice | Wang et al. (2025) |
| αCD40 IgG + systemic recombinant FLT3L protein | C57BL/6 Xcr1DTRVenus | Orthotopic KP2 OVA–expressing models | Intratumoral expansion of total CD8+ T cells, IFNγ+ CD8+ T cells, and therapeutic benefit following treatment was diminished in the absence of cDC1s. Additionally, cDC1 numbers in TME following treatment may be sustained via IFNγ signaling | Hogg et al. (2025) |
| αCD40 IgG + systemic recombinant FLT3L protein | Batf3−/− C57BL/6J | WT- and Mlh1-deficient KP NSCLC SC models | Therapeutic strategy to boost DC prevalence and activation via FLT3L and αCD40 IgG delivery exhibits diminished efficacy in cDC1-deficient mice, associated with diminished CD8+ T cell infiltration into tumor | López et al. (2024) |
| Bispecific antibodies targeting CD40 and DC/cDC1 cell surface markers | Batf3−/− C57BL/6J Xcr1-iDTR | MC38 SC, B16-OVA SC, and MCA-205 SC models | cDC1s are responsible for therapeutic efficacy of therapy but are not implicated in toxicity αCD40-targeted treatment does not induce tumor-specific CD8+ T cells, or therapeutic efficacy in Batf3−/− mice | Salomon et al. (2022) |
| N/A | Xcr1Cre/+Cd40fl/fl (cDC1-specific CD40 deletion) | 1956-mOVA fibrosarcoma SC model | Loss of CD40 signaling in cDC1 diminishes (1) endogenous antitumor CD8+ T cell responses due to lack of cDC1 licensing, (2) early CD4+ T cell activation | Ferris et al. (2020) |
| αCD40 IgG + αPD-1/CTLA4 IgG | B6.129S(C)-Batf3tm1Kmm/J | PDA SC model | Therapeutic efficacy was ablated in Batf3−/− mice | Morrison et al. (2020) |
| αCD40 IgG + gemcitabine/Nab-paclitaxel chemotherapy | Batf3−/− C57BL/6J | PDA SC model | Therapeutic efficacy was diminished in Batf3−/− mice | Byrne and Vonderheide (2016) |
| Oncolytic virus therapy | ||||
| Oral reovirus therapy | B6.129S(C)-Batf3tm1Kmm/J | CT26 SC models | Demonstrates the efficacy of oral delivery of oncolytic virus for, with effects dependent on cDC1s, type I IFN signaling and CD8+ T cells. Oral delivery was not therapeutically effective in cDC1-deficient mice | Lee et al. (2024b) |
| Intratumoral recombinant FLT3L and oncolytic NDV delivery | Batf3−/− BALB/C | A20 SC models | Therapeutic synergy observed between intratumoral recombinant FLT3L delivery and intratumoral NDV delivery. Synergistic effects absent in cDC1-deficient mice Lack of therapeutic efficacy in cDC1-deficient mice associated with lack of induction of tumor-specific T cells | Svensson-Arvelund et al. (2022) |
| Intratumoral delivery of heat-inactivated or live oncolytic vaccinia virus engineered to express GM-CSF | Batf3−/− C57BL/6J | B16 ID models | cDC1s required for antitumor effects of both live and inactivated oncolytic virus delivery | Wang et al. (2021) |
| Intratumoral delivery of inactivated modified vaccine virus Ankara | Batf3−/− C57BL/6J | B16 ID models | Therapeutic efficacy was dependent on cDC1s and additionally STING signaling in host. cDC1s required for induction of tumor-specific CD8+ T cell responses following therapy | Dai et al. (2017) |
| ACT | ||||
| ACT cells expressing XCL1, FLT3L, or combination of both (ACT-FX) | Batf3−/−C57BL/6N | B16-OVA and MC-38 OVA SC models | cDC1s required for efficacy of WT ACT or XCL1-expressing ACT. Additionally, ACT-FX were most effective at controlling tumor growth associated with enhanced DC:T cell interactions in the TME | Xiao et al. (2025) |
| ACT of OT-I cells | XCR1-DTR-Venus C57BL/6J | B16-OVA and MC-38 SC models | cDC1 depletion impaired the efficacy of ACT utilizing OT-I cells associated with decreased intratumoral infiltration, decreased stemness, and increased expression of exhaustion markers | Teijeira et al. (2022) |
| ACT of TYRP1-targeted CAR-T cells alone or in therapeutic combination with STING agonism | Batf3−/− | B16 SC models | cDC1 depletion impaired the efficacy of CAR-T therapy ± STING agonism associated with a loss of epitope spreading and associated expansion of tumor-directed endogenous CD8+ T cell responses | Conde et al. (2021) |
| ACT of CAR-T cells expressing FLT3L in combination with poly I:C treatment | N/A | E0771-OVA-Her2 & MC38-Her2 SC models | CAR-T cells engineered to express FLT3L, given alongside poly I:C and α4-1BB IgG, promoted more effective tumor control, associated with expansion of cDC1, cDC2 populations in the TME and induction of epitope spreading in treated mice | Lai et al. (2020) |
| ACT of CD40L-overexpressing CAR-T cells | Batf3−/− BALB/C | Systemic A20 lymphoma model | Therapeutic efficacy diminished in Batf3−/− mice. Differentiation and expansion of cDC1s in the TME noted in response to ACT | Kuhn et al. (2020) |
| ACT of Pmel-1 CD8+ T cells alone and in combination with hgp100 peptide vaccination | Batf3−/− C57BL/6J | B16 SC model | Expansion of transferred cells was absent in Batf3−/− mice. Utilizing bone chimera models, authors confirm role for CD40 and CD70 signaling in host BATF3-reliant cells for ACT expansion and efficacy | Oba et al. (2020) |
| ACT of CD8+ T cells isolated from matched 2C donor mice and subsequently activated ex vivo | CD11c-DTR/Batf3−/− | Autochthonous BP, BP-SIY, BPC-SIY melanoma models | CD103+ BATF3-dependent cells in the TME produce CXCL9/10 that promote intratumoral infiltration of transferred cells | Spranger et al. (2017) |
| ACT of OT-I cells | XCR1-DTR:Ccr7−/− mixed BM chimeras | B78ChOVA SC model | CCR7-dependent migration of CD103+ DCs is required in the dLN to effectively prime previously transferred antitumor T cells | Roberts et al. (2016) |
| ACT of OT-I cells | FTY720-treated zDC-DTR mice | EG7.1 SC model | CD103+ DCs in tumor are required for antitumor effect of ACT | Broz et al. (2014) |
| cDC1-based vaccination | ||||
| Intratumoral vaccination with peptide-loaded/activated CD34+ HSC-derived human cDC1s in combination with systemic anti–PD-1 IgG | N/A | SC humanized A375 melanoma model | Establishes the therapeutic feasibility and efficacy of a scalable, serum-free platform for generation of bona fide cDC1 from CD34+ progenitors. Intratumoral delivery of activated, antigen-loaded cDC1s combined with anti-PD-1 treatment reduced tumor growth in a humanized melanoma model | Balan et al. (2025) |
| Vaccination with splenic cDC1 or cDC2 loaded with tumor cell lysate via UV-irradiated tumor cells and stimulated with CpG ex vivo | N/A | SC B16-OVA and MC38 | cDC1 vaccination more effective than cDC2 based in delaying tumor growth/prolonging survival and induction of Th1 and CD8+ T cell effector and memory responses | Heras-Murillo et al. (2025) |
| Intratumoral cDC1 vaccination in combination with αPD-1 IgG. XCR1+ cDC1s isolated from the spleen of mice harboring B16-FLT3L tumors were utilized. cDC1s were treated with poly I:C and tumor antigen peptides prior to delivery | N/A | Orthotopic MOC1esc1 (HNSCC model) | Intratumoral cDC1 vaccination restored αPD-1 responsiveness associated with expansion of tumor antigen–specific response and intratumoral infiltration | Saito et al. (2024) |
| Antigen agonistic approach involving intratumoral vaccination with cDC1, cDC2, or GM-CSF/IL-4–cultured DCs | N/A | 1956 mOVA SC model | cDC1-based vaccination outperformed cDC2 or GM-CSF/IL-4 DCs in terms of tumor control and induction of tumor-specific CD8+ T cell responses. Vaccination was only effective via intratumoral and not intravenous route. cDC1-based vaccination was not reliant on the presence of host cDC1s | Ferris et al. (2022) |
| Intratumoral delivery of autologous CD141+ combined with αPD-1 IgG in humanized mouse model | N/A | Humanized mouse model—LM-MEL28 human melanoma cell line | Vaccination of humanized mouse autologous CD141+ DCs (previously activated with poly I:C) synergizes with αPD-1 therapy | Lee et al. (2021) |
| Vaccination with in vitro generated, tumor antigen–loaded, and poly I:C-activated CD103+ DCs alone and in combination with αPD-1 or αCTLA4 IgG | N/A | B16 and K7M3 (osteosarcoma) SC and metastatic models | CD103+ DC-based vaccination outperformed moDC-based vaccination in delaying tumor growth and inducing tumor-specific T cell responses. CD103+ cDC1 vaccination exhibited therapeutic synergy with ICB approaches | Zhou et al. (2020) |
| Vaccination with splenic cDC1 loaded with tumor cell lysate via UV-irradiated tumor cells and stimulated with poly I:C ex vivo | N/A | B16, B16-OVA, and MC38 SC models | First study to demonstrate the efficacy of cDC1-based cancer vaccination. Vaccination with dead tumor cell–loaded cDC1s promoted therapeutic efficacy alone and synergized with PD-1–directed ICB | Wculek et al. (2019) |
| Vaccination with DCs isolated from LLC-OVA tumors: cDC2 (MHC class II+ CD11c+ CD64− CD24− CD11b+ Ly6Clo), cDC1 (MHC class II+, CD11c+ CD64− CD24+ CD11blo) | N/A | B16-OVA, LLC-OVA SC models | cDC1-based vaccination promoted strong induction of antitumor cytotoxic CD8+ T cells cDC1-based vaccination outperformed cDC2-based approaches in the B16-OVA tumor model cDC2-based vaccination outperformed cDC1-based approaches in the LLC-OVA tumor model, with authors hypothesizing role of MDSCs and TAMs in TME mediating lack of cDC1 efficacy | Laoui et al. (2016) |
| Immunotherapy approach | Genetic model utilized | Tumor model utilized | Key findings | Reference |
|---|---|---|---|---|
| αCXCR4 + αPD-1 IgG combination | Orthotopic (HCA-1) and autochthonous HCC models | cDC1 prevalence and proximity to CD8+ T cells increased following combination therapy. Combination therapy effectiveness was compromised in KO mice | ||
| αPD-L1 IgG | Chimeric mice: BM from CD11c-DTR-eGFP mice mixed with WT or | B16-SIY and MC8-SIY SC models | Presence of cDC1s in the TME expressing the costimulatory molecule 4-1BBL required for optimal response to anti-PD-1 blockade | |
| αPD-1 + α4-1BB IgG combination | C57BL/6 XCR1DTRVenus | MC38 SC model | cDC1 depletion impaired therapeutic efficacy associated with reduced intratumoral T cell infiltration | |
| αPD-1 + αCTLA4 IgG alone and in combination | C57BL/6 | E0771 SC model | cDC1 depletion impaired therapeutic efficacy | |
| αCTLA4 IgG | Orthotopic MOSC1 tongue tumor model | αCTLA4-targeted therapy resulted in increase of cDC1s in tdLN. Therapeutic response was diminished in | ||
| αPD-1 IgG + CCL7 combination | N/A | Autochthonous | Combined treatment prolonged survival of mice compared with untreated and PD-1 treatment alone. Therapeutic efficacy was associated with increased infiltration of cDC1s and CD8+ T cells | |
| αPD-L1 IgG | CD11c-Cre; Pdl1^fl/f and | MC38 and EG.7 SC models | PD-L1 expression on DCs essential for response to αPD-L1–targeted therapy. Efficacy of αPD-L1–targeted therapy was diminished in | |
| - | PD-L1–deficient and PD-L1–sufficient MC38, and HEPA1-6.X1.1 SC models | Deletion of PD-L1 expression on DCs, and not macrophages, leads to restriction of tumor growth and enhanced antitumor T cell responses. | ||
| αPD-1 + α4-1BB IgG | Orthotopic 4T1.2 mammary carcinoma model | Adjuvant or neoadjuvant immunotherapy efficacy was diminished in | ||
| αPD-1 IgG | MC38 SC model | Efficacy of αPD-1–targeted therapy was impaired when DCs were depleted or when IL-12 was neutralized. Authors demonstrate a role for IL-12+ cDC1s for optimal therapeutic response | ||
| αPD-L1 IgG | B16 SC models | Efficacy of αPD-L1–targeted therapy was diminished in | ||
| αPD-1 + α4-1BB IgG alone and in combination | MC38, MC38-OVA, and B16-OVA SC models | Efficacy of each immunotherapeutic approach trialed was diminished in | ||
| Systemic α4-1BB IgG in combination with intratumoral HMGN1 (TLR4 agonist) and 3M-052 (TLR7/8 agonist) ISV | MC38 SC models | Combination therapy efficacy was diminished in | ||
| αCD40 IgG + systemic recombinant FLT3L protein | C57BL/6 | Orthotopic KP2 OVA–expressing models | Intratumoral expansion of total CD8+ T cells, IFNγ+ CD8+ T cells, and therapeutic benefit following treatment was diminished in the absence of cDC1s. Additionally, cDC1 numbers in TME following treatment may be sustained via IFNγ signaling | |
| αCD40 IgG + systemic recombinant FLT3L protein | WT- and | Therapeutic strategy to boost DC prevalence and activation via FLT3L and αCD40 IgG delivery exhibits diminished efficacy in cDC1-deficient mice, associated with diminished CD8+ T cell infiltration into tumor | ||
| Bispecific antibodies targeting CD40 and DC/cDC1 cell surface markers | MC38 SC, B16-OVA SC, and MCA-205 SC models | cDC1s are responsible for therapeutic efficacy of therapy but are not implicated in toxicity | ||
| N/A | 1956-mOVA fibrosarcoma SC model | Loss of CD40 signaling in cDC1 diminishes (1) endogenous antitumor CD8+ T cell responses due to lack of cDC1 licensing, (2) early CD4+ T cell activation | ||
| αCD40 IgG + αPD-1/CTLA4 IgG | B6.129S(C)- | PDA SC model | Therapeutic efficacy was ablated in | |
| αCD40 IgG + gemcitabine/Nab-paclitaxel chemotherapy | PDA SC model | Therapeutic efficacy was diminished in | ||
| Oral reovirus therapy | B6.129S(C)- | CT26 SC models | Demonstrates the efficacy of oral delivery of oncolytic virus for, with effects dependent on cDC1s, type I IFN signaling and CD8+ T cells. Oral delivery was not therapeutically effective in cDC1-deficient mice | |
| Intratumoral recombinant FLT3L and oncolytic NDV delivery | A20 SC models | Therapeutic synergy observed between intratumoral recombinant FLT3L delivery and intratumoral NDV delivery. Synergistic effects absent in cDC1-deficient mice | ||
| Intratumoral delivery of heat-inactivated or live oncolytic vaccinia virus engineered to express GM-CSF | B16 ID models | cDC1s required for antitumor effects of both live and inactivated oncolytic virus delivery | ||
| Intratumoral delivery of inactivated modified vaccine virus Ankara | B16 ID models | Therapeutic efficacy was dependent on cDC1s and additionally STING signaling in host. cDC1s required for induction of tumor-specific CD8+ T cell responses following therapy | ||
| ACT cells expressing XCL1, FLT3L, or combination of both (ACT-FX) | B16-OVA and MC-38 OVA SC models | cDC1s required for efficacy of WT ACT or XCL1-expressing ACT. Additionally, ACT-FX were most effective at controlling tumor growth associated with enhanced DC:T cell interactions in the TME | ||
| ACT of OT-I cells | XCR1-DTR-Venus C57BL/6J | B16-OVA and MC-38 SC models | cDC1 depletion impaired the efficacy of ACT utilizing OT-I cells associated with decreased intratumoral infiltration, decreased stemness, and increased expression of exhaustion markers | |
| ACT of TYRP1-targeted CAR-T cells alone or in therapeutic combination with STING agonism | B16 SC models | cDC1 depletion impaired the efficacy of CAR-T therapy ± STING agonism associated with a loss of epitope spreading and associated expansion of tumor-directed endogenous CD8+ T cell responses | ||
| ACT of CAR-T cells expressing FLT3L in combination with poly I:C treatment | N/A | E0771-OVA- | CAR-T cells engineered to express FLT3L, given alongside poly I:C and α4-1BB IgG, promoted more effective tumor control, associated with expansion of cDC1, cDC2 populations in the TME and induction of epitope spreading in treated mice | |
| ACT of CD40L-overexpressing CAR-T cells | Systemic A20 lymphoma model | Therapeutic efficacy diminished in | ||
| ACT of Pmel-1 CD8+ T cells alone and in combination with hgp100 peptide vaccination | B16 SC model | Expansion of transferred cells was absent in | ||
| ACT of CD8+ T cells isolated from matched 2C donor mice and subsequently activated | CD11c-DTR/ | Autochthonous BP, BP-SIY, BPC-SIY melanoma models | CD103+ BATF3-dependent cells in the TME produce CXCL9/10 that promote intratumoral infiltration of transferred cells | |
| ACT of OT-I cells | XCR1-DTR: | B78ChOVA SC model | CCR7-dependent migration of CD103+ DCs is required in the dLN to effectively prime previously transferred antitumor T cells | |
| ACT of OT-I cells | FTY720-treated zDC-DTR mice | EG7.1 SC model | CD103+ DCs in tumor are required for antitumor effect of ACT | |
| Intratumoral vaccination with peptide-loaded/activated CD34+ HSC-derived human cDC1s in combination with systemic anti–PD-1 IgG | N/A | SC humanized A375 melanoma model | Establishes the therapeutic feasibility and efficacy of a scalable, serum-free platform for generation of bona fide cDC1 from CD34+ progenitors. Intratumoral delivery of activated, antigen-loaded cDC1s combined with anti-PD-1 treatment reduced tumor growth in a humanized melanoma model | |
| Vaccination with splenic cDC1 or cDC2 loaded with tumor cell lysate via UV-irradiated tumor cells and stimulated with CpG | N/A | SC B16-OVA and MC38 | cDC1 vaccination more effective than cDC2 based in delaying tumor growth/prolonging survival and induction of Th1 and CD8+ T cell effector and memory responses | |
| Intratumoral cDC1 vaccination in combination with αPD-1 IgG. XCR1+ cDC1s isolated from the spleen of mice harboring B16-FLT3L tumors were utilized. cDC1s were treated with poly I:C and tumor antigen peptides prior to delivery | N/A | Orthotopic MOC1esc1 (HNSCC model) | Intratumoral cDC1 vaccination restored αPD-1 responsiveness associated with expansion of tumor antigen–specific response and intratumoral infiltration | |
| Antigen agonistic approach involving intratumoral vaccination with cDC1, cDC2, or GM-CSF/IL-4–cultured DCs | N/A | 1956 mOVA SC model | cDC1-based vaccination outperformed cDC2 or GM-CSF/IL-4 DCs in terms of tumor control and induction of tumor-specific CD8+ T cell responses. Vaccination was only effective via intratumoral and not intravenous route. cDC1-based vaccination was not reliant on the presence of host cDC1s | |
| Intratumoral delivery of autologous CD141+ combined with αPD-1 IgG in humanized mouse model | N/A | Humanized mouse model—LM-MEL28 human melanoma cell line | Vaccination of humanized mouse autologous CD141+ DCs (previously activated with poly I:C) synergizes with αPD-1 therapy | |
| Vaccination with | N/A | B16 and K7M3 (osteosarcoma) SC and metastatic models | CD103+ DC-based vaccination outperformed moDC-based vaccination in delaying tumor growth and inducing tumor-specific T cell responses. CD103+ cDC1 vaccination exhibited therapeutic synergy with ICB approaches | |
| Vaccination with splenic cDC1 loaded with tumor cell lysate via UV-irradiated tumor cells and stimulated with poly I:C | N/A | B16, B16-OVA, and MC38 SC models | First study to demonstrate the efficacy of cDC1-based cancer vaccination. Vaccination with dead tumor cell–loaded cDC1s promoted therapeutic efficacy alone and synergized with PD-1–directed ICB | |
| Vaccination with DCs isolated from LLC-OVA tumors: cDC2 (MHC class II+ CD11c+ CD64− CD24− CD11b+ Ly6Clo), cDC1 (MHC class II+, CD11c+ CD64− CD24+ CD11blo) | N/A | B16-OVA, LLC-OVA SC models | cDC1-based vaccination promoted strong induction of antitumor cytotoxic CD8+ T cells | |
ACT, adoptive cell therapy; TME, tumor microenvironment; NSCLC, non–small-cell lung cancer; BM, bone marrow; SC, subcutaneous; PDA, pancreatic ductal adenocarcinoma; NDV, Newcastle disease virus.
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