Autologous, ex vivo–prepared dendritic cells (1×10^7 cells) administered post–radical surgery to induce tumor-specific T-cell immunity (CD8+ cytotoxic and CD4+ helper responses) via antigen presentation and costimulation; intended to prevent recurrence/metastasis in survivin- or p53-positive solid tumors.
Autologous ex vivo–prepared dendritic cells present tumor antigens (e.g., survivin/p53) via MHC I/II with costimulatory signals (CD80/CD86) to activate tumor-specific CD8+ cytotoxic and CD4+ helper T cells, enhancing Th1/CTL responses to eliminate residual disease and prevent recurrence/metastasis.
YES
INDIRECT
DC vaccine primes/expands p53-specific CD8+ T cells; CTLs recognize p53-derived peptides on MHC I of tumor cells and kill them via perforin/granzyme (and Fas–FasL) apoptosis.
CD20×CD3 bispecific T‑cell–engaging antibody that redirects T cells to kill CD20+ B cells; administered IV with step‑up dosing.
Glofitamab is a CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to form an immune synapse and activate T cells, leading to perforin/granzyme‑mediated killing of CD20‑positive B‑cell malignancies.
NO
INDIRECT
Glofitamab binds CD3ε on T cells to activate and redirect them; the activated T cells kill CD20+ B cells via perforin/granzyme, not the CD3ε-expressing T cells.
An autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy in which patient T cells are genetically modified to express a CAR targeting CD19, leading to T-cell activation, proliferation, cytokine release, and cytolysis of CD19+ B cells when infused intravenously.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B cells, CAR signaling (CD3 zeta with co-stimulatory domains) activates the T cells, inducing proliferation, cytokine release, and cytolytic killing of CD19-positive malignant and normal B cells.
YES
DIRECT
CD19-specific CAR T cells bind CD19 on B cells, become activated, and kill target cells via perforin/granzyme-mediated cytolysis and apoptosis (with contributions from death receptor and cytokine pathways).
Investigational T-cell–redirecting biologic targeting human kallikrein-2 (KLK2) to direct T cells to lyse KLK2-expressing tumor cells.
Humanized IgG1 bispecific T-cell–redirecting antibody that binds KLK2 on tumor cells and CD3 on T cells, crosslinking them to activate and redirect T-cell cytotoxicity, resulting in lysis of KLK2-expressing tumor cells (notably in prostate cancer).
YES
DIRECT
Bispecific T‑cell–redirecting antibody binds KLK2 on tumor cells and CD3 on T cells, forming a cytolytic synapse and activating T cells to kill KLK2+ cells via perforin/granzyme-mediated lysis.
Investigational T-cell–redirecting biologic targeting human kallikrein-2 (KLK2) to direct T cells to lyse KLK2-expressing tumor cells.
Humanized IgG1 bispecific T-cell–redirecting antibody that binds KLK2 on tumor cells and CD3 on T cells, crosslinking them to activate and redirect T-cell cytotoxicity, resulting in lysis of KLK2-expressing tumor cells (notably in prostate cancer).
NO
INDIRECT
The bispecific antibody binds CD3 on T cells to activate and redirect them toward KLK2-expressing tumor cells; activated T cells mediate perforin/granzyme-dependent lysis of KLK2+ tumor cells. CD3+ cells (T cells) are not killed.