Autologous CD19-directed CAR T cells (19-28z CAR with CD28 and CD3ζ signaling domains) engineered to secrete IL-12; includes a truncated EGFR (EGFRt) tag for tracking and potential cetuximab-mediated depletion.
Autologous T cells engineered with an anti-CD19 CAR containing CD28 and CD3zeta signaling domains recognize CD19 on B-cell malignancies, become activated, proliferate, and kill targets via cytotoxic effector mechanisms. The cells are further engineered to secrete IL-12, which enhances Th1/IFN-gamma responses, activates NK cells, and augments cytotoxic T-cell activity to strengthen antitumor immunity. A truncated EGFR (EGFRt) tag enables in vivo tracking and optional depletion of the cells via cetuximab-mediated ADCC as a safety switch.
NO
INDIRECT
This CAR T therapy targets CD19 and kills CD19+ cells via T‑cell cytotoxicity; secreted IL‑12 signals through IL‑12Rβ1 to activate immune cells but does not target IL‑12Rβ1‑expressing cells for killing.
Autologous CD19-directed CAR T cells (19-28z CAR with CD28 and CD3ζ signaling domains) engineered to secrete IL-12; includes a truncated EGFR (EGFRt) tag for tracking and potential cetuximab-mediated depletion.
Autologous T cells engineered with an anti-CD19 CAR containing CD28 and CD3zeta signaling domains recognize CD19 on B-cell malignancies, become activated, proliferate, and kill targets via cytotoxic effector mechanisms. The cells are further engineered to secrete IL-12, which enhances Th1/IFN-gamma responses, activates NK cells, and augments cytotoxic T-cell activity to strengthen antitumor immunity. A truncated EGFR (EGFRt) tag enables in vivo tracking and optional depletion of the cells via cetuximab-mediated ADCC as a safety switch.
NO
INDIRECT
This CAR T product kills CD19+ cells via CAR-mediated cytotoxicity (perforin/granzyme). IL-12 secretion acts on IL-12Rβ2-expressing immune cells to enhance immunity, not to target them for killing.
Autologous CD19-directed CAR T cells (19-28z CAR with CD28 and CD3ζ signaling domains) engineered to secrete IL-12; includes a truncated EGFR (EGFRt) tag for tracking and potential cetuximab-mediated depletion.
Autologous T cells engineered with an anti-CD19 CAR containing CD28 and CD3zeta signaling domains recognize CD19 on B-cell malignancies, become activated, proliferate, and kill targets via cytotoxic effector mechanisms. The cells are further engineered to secrete IL-12, which enhances Th1/IFN-gamma responses, activates NK cells, and augments cytotoxic T-cell activity to strengthen antitumor immunity. A truncated EGFR (EGFRt) tag enables in vivo tracking and optional depletion of the cells via cetuximab-mediated ADCC as a safety switch.
NO
INDIRECT
EGFRt is a safety tag; the CAR T cells do not target EGFR. EGFRt+ cells would only be depleted if cetuximab is given, triggering NK-cell ADCC against the tagged CAR T cells.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
Allogeneic double-negative T cells express NKG2D; engagement with MICA on target cells triggers MHC-independent cytotoxic degranulation (perforin/granzyme) and IFN-gamma release, leading to tumor cell lysis.
Off-the-shelf allogeneic double-negative T-cell (CD3+ CD4- CD8-) therapy sourced from healthy donors for adoptive cellular immunotherapy after allo-HSCT in high-risk AML; donor DNTs exert MHC-independent cytotoxicity against AML blasts to enhance graft-versus-leukemia and reduce relapse.
Off‑the‑shelf allogeneic double‑negative T cells (CD3+ CD4− CD8−) expanded ex vivo kill AML blasts in an MHC‑independent manner by recognizing NKG2D (KLRK1) and DNAM‑1 (CD226) ligands, releasing IFN‑γ and cytotoxic effectors to augment graft‑versus‑leukemia activity and reduce post‑allo‑HSCT relapse.
YES
DIRECT
Allogeneic double-negative T cells express NKG2D, which binds MICB (an NKG2D ligand) on target cells, triggering MHC-independent cytotoxicity via perforin/granzyme-mediated lysis and IFN-gamma release.