Autologous adoptive T-cell therapy consisting of ex vivo expanded, tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes; administered after lymphodepletion to mediate antigen-specific cytotoxicity.
Autologous tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes are expanded ex vivo and reinfused after lymphodepletion. These unengineered T cells recognize tumor antigens via their native TCRs in an MHC‑restricted manner, expand (with IL‑2 support), and mediate antigen‑specific cytotoxicity through perforin/granzyme release and cytokine production to eliminate tumor cells.
Infused tumor-reactive T cells recognize the tumor-associated peptide–HLA class I complex via their native TCRs and directly kill the presenting cell through perforin/granzyme-mediated apoptosis (± Fas–FasL).
Autologous adoptive T-cell therapy consisting of ex vivo expanded, tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes; administered after lymphodepletion to mediate antigen-specific cytotoxicity.
Autologous tumor‑reactive T lymphocytes harvested from tumor‑draining lymph nodes are expanded ex vivo and reinfused after lymphodepletion. These unengineered T cells recognize tumor antigens via their native TCRs in an MHC‑restricted manner, expand (with IL‑2 support), and mediate antigen‑specific cytotoxicity through perforin/granzyme release and cytokine production to eliminate tumor cells.
Tumor-reactive T cells recognize the specific tumor peptide–HLA class II complex via their native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Anti-CD20 chimeric monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Binding to CD20 on B cells triggers Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and CD20 crosslinking–induced apoptosis.
Anti-CD30 antibody–drug conjugate (ADC) linked to MMAE; binds CD30 on malignant T cells, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis (possible bystander effect).
Anti-CD30 monoclonal antibody linked via a cleavable valine-citrulline linker to MMAE; upon binding CD30 and internalization, MMAE is released to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis (with potential bystander effect).
Anti-CD30 ADC binds CD30, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis (with possible bystander effect).
An intravenous anti-BAFF receptor (BAFF-R) monoclonal antibody that blocks BAFF signaling, depletes B cells, and reduces autoantibody production.
Monoclonal antibody against BAFF receptor (BAFF-R) that blocks BAFF signaling and depletes B cells (via Fc-mediated cytotoxicity), reducing autoreactive B-cell survival and autoantibody production.
Ianalumab binds BAFF-R on B cells and, via its Fc, engages immune effectors to trigger ADCC/ADCP (and CDC), leading to depletion of BAFF-R–expressing cells.