Maternal CMV-specific cytotoxic T lymphocytes used as adoptive cellular immunotherapy; generated/selected with CMV peptide pools to recognize CMV peptide–HLA complexes on infected cells and mediate antigen-specific killing via perforin/granzyme and IFN-γ, restoring antiviral immunity.
Adoptively transferred maternal cytotoxic T lymphocytes selected/expanded for native TCR recognition of CMV peptide–HLA complexes on infected cells; upon engagement they mediate antigen-specific killing via perforin/granzyme release and secrete cytokines (e.g., IFN-γ), restoring CMV-specific cellular immunity without genetic engineering.
Adoptively transferred CMV-specific CTLs recognize CMV pp65 peptide–HLA I via their native TCR and kill target cells by releasing cytotoxic granules (perforin/granzymes) leading to apoptosis (and possibly Fas/FasL signaling).
Maternal CMV-specific cytotoxic T lymphocytes used as adoptive cellular immunotherapy; generated/selected with CMV peptide pools to recognize CMV peptide–HLA complexes on infected cells and mediate antigen-specific killing via perforin/granzyme and IFN-γ, restoring antiviral immunity.
Adoptively transferred maternal cytotoxic T lymphocytes selected/expanded for native TCR recognition of CMV peptide–HLA complexes on infected cells; upon engagement they mediate antigen-specific killing via perforin/granzyme release and secrete cytokines (e.g., IFN-γ), restoring CMV-specific cellular immunity without genetic engineering.
Adoptively transferred CMV-specific CTLs recognize CMV IE1 (UL123) peptide–HLA class I via their TCR and kill the presenting cell by perforin/granzyme-mediated apoptosis (and possibly Fas–FasL).
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19, enabling MHC-independent recognition and activation to proliferate, release cytotoxic effectors and cytokines, and deplete CD19+ malignant and normal B cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells. CAR engagement activates T cells independently of MHC, driving proliferation, cytokine release, and cytotoxic killing (perforin/granzymes) of CD19-positive malignant and normal B cells, leading to B-cell depletion.
CAR T cells bind CD19 and directly kill CD19+ cells via T-cell cytotoxicity (perforin/granzymes and Fas/FasL-mediated apoptosis).
Oral, small-molecule, ATP-competitive HER2 (ERBB2) tyrosine-kinase inhibitor with CNS penetration; suppresses HER2 signaling and downstream PI3K/AKT and MAPK pathways.
Selective oral, ATP-competitive HER2 (ERBB2) tyrosine-kinase inhibitor that blocks HER2 phosphorylation and downstream PI3K/AKT and MAPK signaling; CNS-penetrant, leading to inhibition of growth and survival of HER2-positive tumor cells.
Tucatinib directly inhibits HER2 kinase activity, blocking HER2 phosphorylation and downstream PI3K/AKT and MAPK signaling, leading to growth arrest and apoptosis of HER2-expressing tumor cells.
Anti-HER2 IgG1 monoclonal antibody that blocks HER2 signaling, promotes receptor downregulation, and triggers antibody‑dependent cellular cytotoxicity (engaging NK cells).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); blocks HER2 signaling and dimerization, promotes receptor downregulation, and triggers antibody-dependent cellular cytotoxicity via Fc engagement of NK cells, leading to killing of HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells, triggering antibody‑dependent cellular cytotoxicity (ADCC) that kills HER2+ cells; signaling blockade may also promote apoptosis.