Autologous ex vivo–expanded tumor-infiltrating lymphocyte (TIL) cell therapy enriched for tumor-reactive T cells; mediates anti-tumor activity via TCR recognition and cytotoxic mechanisms (perforin/granzyme) with cytokine secretion.
Autologous ex vivo–expanded tumor-infiltrating T cells that retain native TCRs to recognize patient-specific tumor antigens and mediate anti-tumor effects via cytotoxic granule release (perforin/granzyme) and cytokine secretion, leading to direct tumor-cell killing and immune amplification.
Native TCRs on infused TILs recognize the patient-specific peptide–HLA class I complex and induce target-cell death via cytotoxic granule release (perforin/granzyme–mediated apoptosis), with possible Fas/FasL signaling.
Autologous ex vivo–expanded tumor-infiltrating lymphocyte (TIL) cell therapy enriched for tumor-reactive T cells; mediates anti-tumor activity via TCR recognition and cytotoxic mechanisms (perforin/granzyme) with cytokine secretion.
Autologous ex vivo–expanded tumor-infiltrating T cells that retain native TCRs to recognize patient-specific tumor antigens and mediate anti-tumor effects via cytotoxic granule release (perforin/granzyme) and cytokine secretion, leading to direct tumor-cell killing and immune amplification.
Native TCR recognition of the neoantigen–HLA class II complex on target cells triggers cytotoxic granule release (perforin/granzyme) leading to apoptosis.
Autologous ex vivo–expanded tumor-infiltrating lymphocyte (TIL) cell therapy enriched for tumor-reactive T cells; mediates anti-tumor activity via TCR recognition and cytotoxic mechanisms (perforin/granzyme) with cytokine secretion.
Autologous ex vivo–expanded tumor-infiltrating T cells that retain native TCRs to recognize patient-specific tumor antigens and mediate anti-tumor effects via cytotoxic granule release (perforin/granzyme) and cytokine secretion, leading to direct tumor-cell killing and immune amplification.
Native TCRs on the infused TILs recognize the patient-specific peptide–HLA class II complex and trigger cytotoxic granule release (perforin/granzymes), inducing apoptosis; Fas–FasL can also contribute.
Autologous CD19-directed CAR T-cell therapy that redirects patient T cells to recognize and eliminate CD19-positive B cells.
Autologous T cells genetically engineered to express a CD19-specific chimeric antigen receptor bind CD19 on malignant B cells, triggering T‑cell activation, proliferation, cytokine release, and cytotoxic killing of CD19‑positive cells.
CD19-directed CAR T cells bind CD19 on target cells and induce cytolysis via perforin/granzyme release and death-receptor (Fas/FasL) signaling.
Monoclonal antibody against IL-5 receptor alpha (afucosylated IgG1) that depletes eosinophils via ADCC and blocks IL-5 signaling to reduce eosinophilic inflammation.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha that blocks IL-5 signaling and engages FcγRIIIa to drive potent ADCC, depleting IL-5Rα–expressing eosinophils and basophils to reduce eosinophilic inflammation.
Benralizumab binds IL-5Rα on target cells and engages FcγRIIIa on NK cells, triggering potent ADCC (and related effector functions), leading to apoptosis/depletion of IL-5Rα-expressing eosinophils and basophils.