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1. Publisher Correction: Semaphorin 3A causes immune suppression by inducing cytoskeletal paralysis in tumour-specific CD8+ T cells

2. Semaphorin 3A causes immune suppression by inducing cytoskeletal paralysis in tumour-specific CD8+ T cells

4. MAIT cells activate dendritic cells to promote TFH cell differentiation and induce humoral immunity

5. Discovery of Salmonella trehalose phospholipids reveals functional convergence with mycobacteria

7. Extensive sequence and structural evolution of Arginase 2 inhibitory antibodies enabled by an unbiased approach to affinity maturation

8. Ligand-dependent downregulation of MR1 cell surface expression

9. Chromatin accessibility governs the differential response of cancer and T cells to arginine starvation

10. Hepcidin-Mediated Hypoferremia Disrupts Immune Responses to Vaccination and Infection

11. Semmaphorin 3 A causes immune suppression by inducing cytoskeletal paralysis in tumour-specific CD8+ T cells

13. Sterile activation of invariant natural killer T cells by ER-stressed antigen-presenting cells

15. Deletion of the deISGylating enzyme USP18 enhances tumour cell antigenicity and radiosensitivity

16. Semmaphorin 3 A causes immune suppression by inducing cytoskeletal paralysis in tumour-specific CD8+ T cells

19. Bee venom processes human skin lipids for presentation by CD1a

30. Clonal analysis of Salmonella-specific effector T cells reveals serovar-specific and cross-reactive T cell responses

32. Lipoproteins act as vehicles for lipid antigen delivery and activation of invariant natural killer T-cells

33. Lipoproteins act as vehicles for lipid antigen delivery and activation of invariant natural killer T cells

34. Supplementary File S1 from Enhanced Immunogenicity of Mitochondrial-Localized Proteins in Cancer Cells

35. Supplementary Movie Titles and Legends from Self-Maintaining CD103+ Cancer-Specific T Cells Are Highly Energetic with Rapid Cytotoxic and Effector Responses

36. Data from Enhanced Immunogenicity of Mitochondrial-Localized Proteins in Cancer Cells

37. Movie S1 from Self-Maintaining CD103+ Cancer-Specific T Cells Are Highly Energetic with Rapid Cytotoxic and Effector Responses

38. Supplemental File For Publication from Enriched HLA-E and CD94/NKG2A Interaction Limits Antitumor CD8+ Tumor-Infiltrating T Lymphocyte Responses

39. Supplementary Fig S1-7, Sup Table 1 from Enriched HLA-E and CD94/NKG2A Interaction Limits Antitumor CD8+ Tumor-Infiltrating T Lymphocyte Responses

40. Data from Enriched HLA-E and CD94/NKG2A Interaction Limits Antitumor CD8+ Tumor-Infiltrating T Lymphocyte Responses

41. Data from Self-Maintaining CD103+ Cancer-Specific T Cells Are Highly Energetic with Rapid Cytotoxic and Effector Responses

42. Supplementary Figures 1-7 and Supplementary Tables 1-2 from Self-Maintaining CD103+ Cancer-Specific T Cells Are Highly Energetic with Rapid Cytotoxic and Effector Responses

43. Supplementary Figures and Tables from Enhanced Immunogenicity of Mitochondrial-Localized Proteins in Cancer Cells

44. Data from Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells

45. Supplementary Figure Legends from Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells

46. Figure S4 from Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells

47. Supplementary Materials and Methods from Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells

48. Table S1 from Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells

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