Lack of B7.1 and B7.2 on head and neck cancer cells and possible significance for gene therapy.

Cellular immunity mediated by cytotoxic T-cells plays a key role in host tumor defense. An optimal T-cell recognition is based primarily on the presentation of an antigen in the context with MHC Class I molecules, secondarily co-stimulatory molecules, such as the B7 family, are necessary to initiate maximum stimulation. We examined the quality (immunohistochemically) and quantity (FACS-analysis) of B7 expression on primary and permanently established head and neck squamous cell cancer (HNSCC). Neither on the primary nor on the permanently established HNSCC lines could B7 be detected. The lack of co-stimulatory molecules could be the reason for the low immunogenicity of HNSCC. Future gene transfer of B7 could help to restore the immune function. Transfection of expression plasmids encoding B7 cDNA into the tumor cells by gene therapy might restore tumor-specific immunity as a new tool for cancer eradication in the future.