Skip to main content
Fig. 2 | Experimental Hematology & Oncology

Fig. 2

From: Recent advances and challenges of bispecific antibodies in solid tumors

Fig. 2

The killing mechanism of TrioMabs (taking Catumaxomab as an example). TrioMabs is a trifunctional BsAb with one arm targeting TAA on tumor cells, another arm targeting CD3 on T cells and the Fc domain binding to Fcγ receptor type I, IIa and III on effector cells such as macrophages, dendritic cells, and NK cells. Once the Fc region of BsAb binds to Fcγ receptor expressed by effector cells or complement component 1q (C1q), these effector cells are activated and release perforins and granzymes from its granules, potentially supporting the destruction of target cells through ADCC, ADCP and CDC, respectively [24]. Additionally, T cells are activated, accompanied by the release of T cell cytokines such as TNF-α and IFN-γ with high levels of proinflammatory cytokines such as IL-6, IL-12, GM-CSF, and DC-CK1 [34, 35]

Back to article page