Autologous CMV-specific T cells genetically engineered to express an anti-CD19 chimeric antigen receptor, enabling targeted cytotoxicity against CD19-positive malignant B cells; endogenous CMV-specific TCRs allow antigen-driven recall responses to support in vivo expansion and persistence after transplant.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor that redirects T-cell cytotoxicity to CD19-positive malignant B cells; native CMV-specific TCRs enable antigen-driven recall responses to enhance in vivo expansion and persistence, which can be boosted by CMV vaccination post-transplant.
NO
INDIRECT
CMV peptide antigens engage the native CMV-specific TCRs to restimulate and expand the engineered T cells; actual killing is mediated by the anti-CD19 CAR against CD19+ cells, not by recognition of CMV peptides.
A Modified Vaccinia Ankara (MVA) viral-vector vaccine encoding CMV antigens (Triplex) designed to boost CMV-specific T-cell activation and drive expansion/persistence of CMV-specific CD19-CAR T cells post-transplant.
Non-replicating Modified Vaccinia Ankara (MVA) vector encoding CMV antigens (pp65/IE1/IE2) infects antigen-presenting cells and expresses these proteins, leading to MHC I/II presentation and activation/expansion of CMV-specific CD8+ cytotoxic and CD4+ helper T cells. In this setting, it boosts the in vivo expansion and persistence of CMV-specific CD19-CAR T cells and promotes lysis of CMV-infected cells, helping prevent CMV reactivation.
YES
INDIRECT
The MVA vaccine boosts pp65-specific CD8+ T cells (and supports CMV-specific CAR T cells), which recognize pp65 peptides presented on MHC I of CMV-infected cells and kill them via perforin/granzyme-mediated cytolysis, with CD4+ T-cell help.
A Modified Vaccinia Ankara (MVA) viral-vector vaccine encoding CMV antigens (Triplex) designed to boost CMV-specific T-cell activation and drive expansion/persistence of CMV-specific CD19-CAR T cells post-transplant.
Non-replicating Modified Vaccinia Ankara (MVA) vector encoding CMV antigens (pp65/IE1/IE2) infects antigen-presenting cells and expresses these proteins, leading to MHC I/II presentation and activation/expansion of CMV-specific CD8+ cytotoxic and CD4+ helper T cells. In this setting, it boosts the in vivo expansion and persistence of CMV-specific CD19-CAR T cells and promotes lysis of CMV-infected cells, helping prevent CMV reactivation.
YES
INDIRECT
The MVA vaccine primes/expands CMV IE1-specific CD8+ T cells, which recognize IE1-derived peptides on MHC I of CMV-infected cells and kill them via perforin/granzyme-mediated cytolysis (with CD4+ T-cell help).
A Modified Vaccinia Ankara (MVA) viral-vector vaccine encoding CMV antigens (Triplex) designed to boost CMV-specific T-cell activation and drive expansion/persistence of CMV-specific CD19-CAR T cells post-transplant.
Non-replicating Modified Vaccinia Ankara (MVA) vector encoding CMV antigens (pp65/IE1/IE2) infects antigen-presenting cells and expresses these proteins, leading to MHC I/II presentation and activation/expansion of CMV-specific CD8+ cytotoxic and CD4+ helper T cells. In this setting, it boosts the in vivo expansion and persistence of CMV-specific CD19-CAR T cells and promotes lysis of CMV-infected cells, helping prevent CMV reactivation.
YES
INDIRECT
The MVA vaccine primes/expands IE2-specific CTLs that recognize IE2 peptides on MHC I of CMV-infected cells and kill them via perforin/granzyme-mediated cytolysis (with CD4+ T-cell help); the vaccine itself is not directly cytotoxic.
A CD20×CD3 bispecific monoclonal antibody T‑cell engager that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and drive T‑cell–mediated cytotoxicity against CD20+ lymphoma.
CD20×CD3 bispecific antibody that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling and drives T‑cell–mediated cytotoxicity against CD20‑positive lymphoma cells.
YES
DIRECT
The CD20×CD3 bispecific antibody bridges CD20+ cells to T cells, activating CD3/TCR signaling and inducing perforin/granzyme-mediated killing of the CD20-expressing cells.