Genetically engineered autologous T cells expressing a chimeric antigen receptor targeting CD19, administered once to deplete CD19+ B-lineage cells and reset humoral immunity in refractory SLE/lupus nephritis.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19. When the CAR binds CD19 on B-lineage cells, it triggers T-cell activation (CD3zeta with costimulatory signaling), proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to depletion of CD19+ B cells and plasmablasts, reduction of autoantibody production, and reset of humoral immunity.
YES
DIRECT
CAR T cells bind CD19 via the CAR and directly kill CD19+ cells through T‑cell activation with perforin/granzyme-mediated apoptosis (and death-receptor signaling).
An intradermal plasmid DNA cancer vaccine encoding Th1-biased polyepitopes from CDH3 (P-cadherin), CD105 (endoglin), YB-1, MDM2, and SOX2 to induce antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ responses against NSCLC.
Intradermal plasmid DNA vaccine encoding Th1-biased polyepitopes from CDH3, CD105, YB-1, MDM2, and SOX2 is taken up by antigen-presenting cells, leading to in situ expression, processing, and MHC I/II presentation. This primes antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ helper responses to recognize and kill NSCLC cells expressing these antigens, enhancing tumor-specific cellular immunity.
YES
INDIRECT
The DNA vaccine primes CD8+ T cells against CDH3-derived epitopes; activated CTLs recognize CDH3 peptide–MHC I on tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.
An intradermal plasmid DNA cancer vaccine encoding Th1-biased polyepitopes from CDH3 (P-cadherin), CD105 (endoglin), YB-1, MDM2, and SOX2 to induce antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ responses against NSCLC.
Intradermal plasmid DNA vaccine encoding Th1-biased polyepitopes from CDH3, CD105, YB-1, MDM2, and SOX2 is taken up by antigen-presenting cells, leading to in situ expression, processing, and MHC I/II presentation. This primes antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ helper responses to recognize and kill NSCLC cells expressing these antigens, enhancing tumor-specific cellular immunity.
YES
INDIRECT
The DNA vaccine is taken up by APCs, which present CD105-derived peptides to prime CD8+ T cells; these antigen-specific CTLs then recognize CD105 peptide–MHC I on tumor cells and kill them via perforin/granzyme-mediated apoptosis.
An intradermal plasmid DNA cancer vaccine encoding Th1-biased polyepitopes from CDH3 (P-cadherin), CD105 (endoglin), YB-1, MDM2, and SOX2 to induce antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ responses against NSCLC.
Intradermal plasmid DNA vaccine encoding Th1-biased polyepitopes from CDH3, CD105, YB-1, MDM2, and SOX2 is taken up by antigen-presenting cells, leading to in situ expression, processing, and MHC I/II presentation. This primes antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ helper responses to recognize and kill NSCLC cells expressing these antigens, enhancing tumor-specific cellular immunity.
YES
INDIRECT
The DNA vaccine primes YB-1–specific CD8+ T cells via APC presentation; CTLs then recognize YB-1–derived peptides on MHC I of tumor cells and kill them via perforin/granzyme-mediated apoptosis, supported by Th1 CD4+ help.
An intradermal plasmid DNA cancer vaccine encoding Th1-biased polyepitopes from CDH3 (P-cadherin), CD105 (endoglin), YB-1, MDM2, and SOX2 to induce antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ responses against NSCLC.
Intradermal plasmid DNA vaccine encoding Th1-biased polyepitopes from CDH3, CD105, YB-1, MDM2, and SOX2 is taken up by antigen-presenting cells, leading to in situ expression, processing, and MHC I/II presentation. This primes antigen-specific CD8+ cytotoxic T cells and Th1 CD4+ helper responses to recognize and kill NSCLC cells expressing these antigens, enhancing tumor-specific cellular immunity.
YES
INDIRECT
The DNA vaccine primes MDM2-specific CD8+ T cells; these CTLs recognize MDM2-derived peptides on MHC I of tumor cells and kill them via perforin/granzyme-mediated cytolysis (with Th1 CD4+ help).