Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which patient tumor T cells are expanded ex vivo and reinfused after lymphodepleting chemotherapy to mediate tumor-specific cytotoxicity and enhance persistence.
Autologous T cells isolated from the patient’s tumor are expanded ex vivo and reinfused after lymphodepleting chemotherapy to reconstitute a large pool of tumor‑reactive T cells. These TILs recognize native tumor antigens via their endogenous TCRs and mediate tumor cell killing through cytotoxic effector functions, supporting durable antitumor immunity.
YES
DIRECT
Reinfused TILs recognize the tumor-associated peptide–HLA class II complex via their endogenous TCRs and directly kill the presenting cell through perforin/granzyme release and/or Fas–FasL–mediated apoptosis.
A human IgG1 broadly neutralizing monoclonal antibody engineered with an LS Fc mutation for extended half-life; binds the HIV-1 Env gp120 V2 apex to block viral entry and can mediate Fc-dependent effector functions (ADCC/ADCP).
Human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation for extended half-life (enhanced FcRn binding); binds the HIV-1 Env gp120 V2 apex to neutralize virions and block viral entry, and can engage Fc gamma receptors to mediate ADCC/ADCP against Env-expressing infected cells.
YES
DIRECT
The IgG1 antibody binds the Env gp120 V2 apex on infected cells and engages Fcγ receptors to trigger NK-cell ADCC and macrophage ADCP (and potentially complement/CDC), killing Env-expressing cells.
A human IgG1 broadly neutralizing monoclonal antibody engineered with an LS Fc mutation for extended half-life; binds the HIV-1 Env gp120 V2 apex to block viral entry and can mediate Fc-dependent effector functions (ADCC/ADCP).
Human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation for extended half-life (enhanced FcRn binding); binds the HIV-1 Env gp120 V2 apex to neutralize virions and block viral entry, and can engage Fc gamma receptors to mediate ADCC/ADCP against Env-expressing infected cells.
NO
INDIRECT
PGDM1400LS targets HIV-1 Env, enabling FcγR-mediated ADCC/ADCP against Env-expressing infected cells. Its LS mutation increases FcRn binding for IgG recycling; FcRn-expressing cells are not killed.
A human IgG1 broadly neutralizing monoclonal antibody engineered with an LS Fc mutation for extended half-life; binds the HIV-1 Env gp120 V2 apex to block viral entry and can mediate Fc-dependent effector functions (ADCC/ADCP).
Human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation for extended half-life (enhanced FcRn binding); binds the HIV-1 Env gp120 V2 apex to neutralize virions and block viral entry, and can engage Fc gamma receptors to mediate ADCC/ADCP against Env-expressing infected cells.
NO
INDIRECT
The antibody binds HIV-1 Env on infected cells and engages CD16a on NK cells via its Fc to trigger ADCC, killing Env-expressing target cells rather than CD16a-expressing effector cells.
Lentiviral CAR T cells targeting GPRC5D; IV dose-escalated infusion; mediates MHC-independent killing of GPRC5D+ myeloma cells/plasma cells.
Autologous/allogeneic T cells are lentivirally transduced to express a CAR specific for GPRC5D. Upon binding GPRC5D on malignant plasma cells, the CAR triggers MHC-independent T-cell activation, leading to cytotoxic killing via perforin/granzyme release and cytokine-mediated elimination of GPRC5D-positive myeloma cells.
YES
DIRECT
GPRC5D-specific CAR T cells bind GPRC5D on target cells, become activated, and kill via T-cell cytotoxicity (perforin/granzyme–mediated lysis, with possible Fas/FasL and cytokine-mediated effects).