Patient-derived T cells genetically engineered to express an anti-CD5 chimeric antigen receptor that binds CD5 on malignant T cells and activates CAR-mediated cytotoxicity (CD3zeta/costimulatory signaling), leading to killing of CD5+ tumor cells with expected on-target depletion of normal CD5+ T cells.
Autologous patient T cells are genetically engineered to express a CD5-directed chimeric antigen receptor. Upon binding CD5 on malignant T cells, the CAR transmits activation signals (CD3ζ with costimulatory domains), triggering T-cell cytotoxicity (perforin/granzyme) and elimination of CD5+ tumor cells, with expected on-target depletion of normal CD5+ T cells.
YES
DIRECT
CD5 CAR T cells bind CD5 on target cells, activating CAR signaling and T-cell cytotoxicity (perforin/granzyme-mediated lysis/apoptosis) to kill CD5+ cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
YES
DIRECT
CAR T cells bind CD19 on target cells; CAR/CD3ζ signaling activates T-cell cytotoxicity, leading to perforin/granzyme-mediated apoptosis (with possible Fas/FasL), augmented by IL-15-enhanced activation and persistence.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
YES
DIRECT
Anti-CD22 CAR T cells bind CD22 on target cells, triggering CAR/CD3zeta signaling and T-cell cytolysis via perforin/granzyme (and Fas-FasL) pathways; IL-15 enhances T-cell activation and persistence.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
YES
DIRECT
CAR T cells recognize BCMA via the CAR, triggering CD3ζ signaling and T-cell effector functions that kill BCMA+ cells via perforin/granzyme-mediated cytolysis (with supportive cytokine-mediated apoptosis).
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B-cell antigens (CD19 and/or CD22 for B-ALL/B-NHL or BCMA for multiple myeloma) and to co-express interleukin-15 (IL-15) to enhance T-cell activation, proliferation, survival, and persistence for antitumor cytotoxicity.
Autologous T lymphocytes are engineered to express a chimeric antigen receptor targeting B‑cell antigens (CD19 and/or CD22, or BCMA). Antigen engagement triggers CAR/CD3ζ signaling, leading to T‑cell activation and cytotoxic killing of tumor cells via perforin/granzymes and cytokine release. Co‑expressed IL‑15 delivers autocrine IL‑15R–JAK/STAT signaling that enhances T‑cell activation, proliferation, survival, and persistence, improving antitumor efficacy.
NO
INDIRECT
CAR T cells kill cells expressing CD19/CD22/BCMA via CAR activation and perforin/granzyme release. IL‑15 signals through IL‑15 receptors on the CAR T cells to enhance their function; IL15RA+ cells are not directly targeted or killed.