Immunotherapy for cancer: construction, expression and functional characterization of chimeric antibodies.

Monoclonal antibodies (Mabs) are a potential key component for the treatment of cancer, because of their specificity and multiple effector functions. Hybridoma technology and progress in genetic engineering made it possible to customize antibody molecules, rendering them more suitable for selective application. A widely used technique is the construction of mouse-human hybrid molecules by recombinant DNA techniques.

Mono- and bispecific single-chain antibody fragments for cancer therapy.

Especially when dealing with solid cancers, single-chain antibody fragments (scFvs) have a lot of advantages. Due to their small size (27 kDa), these proteins clear more rapidly from the blood, and penetrate faster and deeper into tissues, than whole antibodies. Furthermore, the lack of constant regions ensures that they are not retained in tissues such as the liver and kidney.

Development and functional characterization of a murine/human chimeric antibody with specificity for the human interleukin-2 receptor.

A murine/human chimeric antibody, with specificity for the human interleukin-2 receptor, was developed by genetic engineering. For this purpose, the light and heavy chain variable region exons encoding the murine monoclonal antibody 2C8 were isolated and inserted into expression vectors containing the human kappa and gamma-1 constant regions. After transfection by electroporation of the chimeric genes into murine Sp 2/0 hybridoma cells, transfectomas secreting the complete chimeric antibody were selected.

Decreased expression of the memory marker CD26 on both CD4+ and CD8+ T lymphocytes of HIV-infected subjects.

Using a novel anti-CD26 (or anti-dipeptidyl peptidase IV) monoclonal antibody, we showed that the absolute numbers and the proportions of T4 and T8 cells expressing CD26 were significantly lower in HIV-infected persons than in controls. The absolute number of CD26+ T4 cells decreased according to disease progression, whereas the number of CD26+ T8 cells was low throughout all clinical stages. These trends were similar in CD26 dim and bright positive T-cell subsets.