Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo and reinfused to mediate patient-specific, TCR-dependent antitumor cytotoxicity.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize patient-specific tumor antigens via their native T-cell receptors and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, often supported by IL-2 to enhance expansion and persistence.
YES
DIRECT
TILs recognize HPV E7 peptide presented on MHC via native TCRs and directly kill tumor cells through perforin/granzyme-mediated cytolysis (with possible Fas–FasL and cytokine effects).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo and reinfused to mediate patient-specific, TCR-dependent antitumor cytotoxicity.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are reinfused to recognize patient-specific tumor antigens via their native T-cell receptors and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, often supported by IL-2 to enhance expansion and persistence.
YES
DIRECT
Autologous TILs recognize tumor-associated antigen peptides presented on MHC via native TCRs and kill target cells through perforin/granzyme-mediated cytotoxicity (with possible Fas–FasL and cytokine effects).
A personalized cancer vaccine composed of patient-specific tumor neoantigens administered subcutaneously to load antigen-presenting cells (primarily dendritic cells), enhance MHC I/II presentation, and expand tumor-specific CD8+ cytotoxic and CD4+ helper T cells to eliminate residual micrometastatic disease and establish immune memory in post-resection stage IIIA lung adenocarcinoma.
Personalized neoantigen peptide vaccine given subcutaneously to be taken up by antigen‑presenting cells (mainly dendritic cells), enhancing MHC I/II presentation and priming/expanding neoantigen‑specific CD8+ cytotoxic and CD4+ helper T cells to eradicate residual tumor cells and establish durable immune memory.
NO
INDIRECT
The vaccine primes/expands neoantigen-specific CD8+ T cells via APC presentation; these T cells kill tumor cells only if they present the specific neoantigen peptide on MHC I (e.g., HLA-B) via perforin/granzyme or Fas. HLA-B expression alone is not targeted.
A human bispecific IgG antibody (anti-BCMA × anti-CD3), also known as REGN5458 and Lynozyfic, administered intravenously. It redirects T cells to kill BCMA-expressing myeloma cells by simultaneously binding BCMA on plasma cells and CD3 on T cells, forming an immune synapse and inducing cytotoxicity.
Linvoseltamab is a human bispecific IgG antibody (anti-BCMA × anti-CD3) that redirects T cells to kill BCMA-expressing myeloma cells by simultaneously binding BCMA on plasma cells and CD3 on T cells, forming an immune synapse that activates T cells and triggers perforin/granzyme-mediated cytotoxicity and cytokine release.
YES
DIRECT
Bispecific anti-BCMA×anti-CD3 redirects T cells to BCMA+ cells, forming an immune synapse that activates T cells to kill via perforin/granzyme-mediated cytotoxicity.
A human bispecific IgG antibody (anti-BCMA × anti-CD3), also known as REGN5458 and Lynozyfic, administered intravenously. It redirects T cells to kill BCMA-expressing myeloma cells by simultaneously binding BCMA on plasma cells and CD3 on T cells, forming an immune synapse and inducing cytotoxicity.
Linvoseltamab is a human bispecific IgG antibody (anti-BCMA × anti-CD3) that redirects T cells to kill BCMA-expressing myeloma cells by simultaneously binding BCMA on plasma cells and CD3 on T cells, forming an immune synapse that activates T cells and triggers perforin/granzyme-mediated cytotoxicity and cytokine release.
NO
INDIRECT
Linvoseltamab uses its anti-CD3 arm to engage and activate T cells; it does not kill CD3+ T cells. Activated T cells then kill BCMA-expressing tumor cells via perforin/granzyme after immune synapse formation.