Fig. 2

The comparison of BiTEs (taking MT110 as an example) and triomabs (taking catumaxomab as an example) killing mechanism. The interaction of T cells and tumor cells, which is mediated by BsAbs, initiates the killing process of T cells, including CD3 activation, formation of immunologic synapses, T-cell activation and proliferation, secretion of cytokines and cytotoxic granules, and tumor cell lysis [19]. The activated CD8⁺ and CD4⁺ T cells lyse cancer cells predominantly through perforin and granzyme B. The activated T cells secrete various cytokines such as IFN-γ, TNF, IL-2, IL-6, and IL-10 [20]. In addition to the above mechanism, triomabs can recruit other immune cells such as NK cells, macrophages which could kill tumor cells and mediate the co-stimulation between T cells and accessory cells [16]. Simultaneously recruiting and activating different immune effector cells to the tumor site result in potent tumor-cell elimination by the above different immunologic killing mechanisms