Figure 1. Immune escape mechanisms of tumour cells. Recognition of tumour cells by T cells requires a tumour-associated peptide (pep) to be presented by a major histocompatibility complex (MHC) molecule and recognition of this peptide–MHC complex by the T-cell receptor (TCR) and ligation with CD4/CD8 molecules. The TCR consists of an chain, and recognition leads to a signal through the CD3 complex (, (two), and (two) chains). To activate the T cell, the signal needs to reach the nucleus through downstream molecules such as p56 lck, p59 fyn and zeta-associated protein of 70 kDa (ZAP-70). Downregulation or inactivation of any of the molecules involved in this cascade will prevent T-cell activation and lead to subsequent killing of the tumour cell. Inability to release peptides from a protein, or to load the peptide on the MHC molecule, will prevent recognition of the tumour cell. Finally, expression of Fas ligand on tumour cells may induce apoptosis (programmed cell death) in the specific T cell, which prevents the tumour cell from being eradicated.

Figure 2. Adoptive transfer refers to the injection of immune cells or antibodies obtained from another source into a naive mouse (host) in order transfer immunity passively to this mouse (host). Most common sources of immune cells are spleens of vaccinated mice or in vitro established T-cell clones. Antibodies can be obtained from serum of vaccinated mice or from monoclonal antibody-producing B cells in vitro.

Figure 3. Bispecific monoclonal antibodies. The fusion of cells that produce a T cell-activating monoclonal antibody with a cell that produces a tumour cell-specific monoclonal antibody will result in a cell that produces bispecific antibodies. The bispecific antibodies bridge the tumour cell with a T cell and hold them together. When the bispecific antibody activates the T cell, the tumour cell will be killed.