Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
YES
DIRECT
TILs use native TCRs to recognize the tumor peptide–HLA-B complex on target cells, triggering cytotoxic T-cell killing via perforin/granzyme release and death receptor pathways (e.g., Fas–FasL).
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
YES
DIRECT
TILs use their native TCRs to recognize tumor antigenic peptide–HLA-C complexes and directly lyse target cells via perforin/granzyme release (and Fas–FasL), with cytokine-mediated support.
A recombinant human broadly neutralizing monoclonal antibody that targets the HIV-1 gp120 V3-glycan (N332) supersite to inhibit viral entry; neutralizes diverse HIV-1 strains and can mediate Fc-dependent effector functions (ADCC/ADCP). The LS Fc mutations enhance FcRn binding and extend serum half-life.
10-1074-LS is a broadly neutralizing human monoclonal antibody that binds the HIV-1 Env gp120 V3-glycan (N332) supersite, blocking Env–CD4 interactions and viral attachment/entry to neutralize diverse HIV-1 strains. Its Fc region can engage Fcγ receptors to mediate effector functions such as ADCC and ADCP, aiding clearance of virions/infected cells. LS Fc mutations (M428L/N434S) enhance FcRn binding, extending serum half-life.
NO
INDIRECT
10-1074-LS binds HIV-1 Env on infected cells; its Fc engages CD16A on NK cells/macrophages to trigger ADCC/ADCP that kills Env-positive infected cells. CD16A-expressing cells are effectors, not targets.
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
YES
DIRECT
TILs recognize the tumor antigenic peptide–HLA-DR complex via their native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis, with supportive cytokine effects.
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
YES
DIRECT
TILs use their native TCRs to recognize the tumor antigenic peptide–HLA-DP complex on target cells and directly kill them via perforin/granzyme release and Fas–FasL–mediated apoptosis.