ABSTRACT
O bservations that susceptibility to several cancer types is increased in immunocompromised individuals have led to the assumption that immune responses are able to interfere with tumor development.1 Early attempts focussed on the gen eral activation of the patient s immune system as a means of cancer therapy, for instance by administration of bacterial extracts, Bacillus Calmette-Guérin, or high dose interleukin-2.2'4
In the last decades, our knowledge on the specificity and regulation of the immune system has expanded tremendously. The major effectors involved in the eradication of tumor cells are likely to be T lymphocytes, which can recognize subtle intracellular changes showing up as antigenic peptides presented by major histocompatibility complex (MHC) class I and class II molecules. MHC class II molecules are mainly found on cells of the immune system with a specialized antigen presenting function, including dendritic cells (DC). Upon triggering by class II/peptide complexes, CD4+ T helper (Th) cells can orchestrate the action of numerous immune cells. MHC class I molecules are expressed on the surface of virtually all nucleated cells and, through these, CD8+ cytotoxic T lymphocytes (CTL) can screen almost all cells of the body for antigenic peptides that may be presented as a consequence of viral infection or malignant transformation. Thus, CTL represent a major effector subset of specific T cells po tentially able to eradicate virus-infected or malignantly transformed cells.
