197 results on '"Sluijter, Marjolein"'
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2. Immunotherapy-activated T cells recruit and skew late-stage activated M1-like macrophages that are critical for therapeutic efficacy
3. The MHC-E peptide ligands for checkpoint CD94/NKG2A are governed by inflammatory signals, whereas LILRB1/2 receptors are peptide indifferent
4. Data from Intertumoral Differences Dictate the Outcome of TGF-β Blockade on the Efficacy of Viro-Immunotherapy
5. Figure S5 from Intertumoral Differences Dictate the Outcome of TGF-β Blockade on the Efficacy of Viro-Immunotherapy
6. Table TS2 from Intertumoral Differences Dictate the Outcome of TGF-β Blockade on the Efficacy of Viro-Immunotherapy
7. Supplementary Methods SM1 from Intertumoral Differences Dictate the Outcome of TGF-β Blockade on the Efficacy of Viro-Immunotherapy
8. Data from CD4+ T Cell and NK Cell Interplay Key to Regression of MHC Class Ilow Tumors upon TLR7/8 Agonist Therapy
9. Fig S3 from CD3-Bispecific Antibody Therapy Turns Solid Tumors into Inflammatory Sites but Does Not Install Protective Memory
10. Figure S1 from CD4+ T Cell and NK Cell Interplay Key to Regression of MHC Class Ilow Tumors upon TLR7/8 Agonist Therapy
11. Supplementary Figure Legends from CD3-Bispecific Antibody Therapy Turns Solid Tumors into Inflammatory Sites but Does Not Install Protective Memory
12. Data from CD3-Bispecific Antibody Therapy Turns Solid Tumors into Inflammatory Sites but Does Not Install Protective Memory
13. Figure legends from CD4+ T Cell and NK Cell Interplay Key to Regression of MHC Class Ilow Tumors upon TLR7/8 Agonist Therapy
14. Supplemental Figure S4 from Therapeutic Peptide Vaccine-Induced CD8 T Cells Strongly Modulate Intratumoral Macrophages Required for Tumor Regression
15. Supplementary Table 1 from Therapeutic Peptide Vaccine-Induced CD8 T Cells Strongly Modulate Intratumoral Macrophages Required for Tumor Regression
16. Data from Therapeutic Peptide Vaccine-Induced CD8 T Cells Strongly Modulate Intratumoral Macrophages Required for Tumor Regression
17. Supplementary Figures S1-S3 from Local Activation of CD8 T Cells and Systemic Tumor Eradication without Toxicity via Slow Release and Local Delivery of Agonistic CD40 Antibody
18. Supplementary Figure 2 from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
19. Supplementary Figure 1 from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
20. Data from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
21. Data from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
22. Supplementary Figure 3 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
23. Supplementary Figure 6 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
24. Supplementary Figure 4 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
25. Supplementary Figure 3 from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
26. Supplementary Figure 4 from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
27. Supplementary Table 1 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
28. Supplementary Figure 2 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
29. Supplementary Figure 1 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
30. Supplementary Figure Legends 1-6 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
31. Supplementary Figure 5 from Design of Agonistic Altered Peptides for the Robust Induction of CTL Directed towards H-2Db in Complex with the Melanoma-Associated Epitope gp100
32. Supplementary Figure Legends 1- 4 from Peptide Vaccination after T-Cell Transfer Causes Massive Clonal Expansion, Tumor Eradication, and Manageable Cytokine Storm
33. Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNγ receptor signaling
34. Intertumoral Differences Dictate the Outcome of TGF-β Blockade on the Efficacy of Viro-Immunotherapy
35. Tumor-nonspecific vaccines improve the efficacy of CD3 bispecific antibody therapy in solid tumors
36. In vivo modelling of cutaneous T-cell lymphoma: The role of SOCS1
37. Effectiveness of slow-release systems in CD40 agonistic antibody immunotherapy of cancer
38. TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors
39. Preinduced reovirus-specific T-cell immunity enhances the anticancer efficacy of reovirus therapy
40. A Single-Domain TCR-like Antibody Selective for the Qa-1b/Qdm Peptide Complex Enhances Tumoricidal Activity of NK Cells via Blocking the NKG2A Immune Checkpoint
41. Targeting pancreatic cancer by TAK-981: a SUMOylation inhibitor that activates the immune system and blocks cancer cell cycle progression in a preclinical model
42. Involvement of several alternative antigen processing routes for the MHC-I presentation of TAP-independent peptides
43. NKG2A is a late immune checkpoint on CD8 T cells and marks repeated stimulation and cell division
44. Dominant contribution of the proteasome and metalloproteinases to TAP-independent MHC-I peptide repertoire
45. Alternative peptide repertoire of HLA-E reveals a binding motif that is strikingly similar to HLA-A2
46. NKG2A is a late immune checkpoint on CD8 T cells and marks repeated stimulation and cell division.
47. Additional file 1: of Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNγ receptor signaling
48. Additional file 2: of Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFNÎł receptor signaling
49. CD3-Bispecific Antibody Therapy Turns Solid Tumors into Inflammatory Sites but Does Not Install Protective Memory
50. A herpesvirus encoded Qa-1 mimic inhibits natural killer cell cytotoxicity through CD94/NKG2A receptor engagement
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