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The role of the immune system in combating tumour progression has been studied extensively. The two branches of the immune response -humoral and cell-mediated -act both independently and in concert to combat tumour progression, the success of which depends on the immunogenicity of the tumour cells. The immune system discriminates between transformed cells and normal cells by virtue of the presence of unique antigens on tumour cells. Despite this, the immune system is not always able to detect and kill cancerous cells because neoplasms have also evolved various strategies to escape immune surveillance. Attempts are being made to trigger the immune system into an early and efficient response against malignant cells, and various therapeutic modalities are being developed to enhance the strength of the immune response against tumours. This review aims to elucidate the tumouricidal role of various components of the immune system, including macrophages, lymphocytes, dendritic cells and complement.

We demonstrate the migration of antigen presenting cells (APCs), macrophages, and dendritic cells from the subcutaneous site to the peritoneum after they have picked up the antigen, using cell tracking dye. The migration of the APCs is more universal as it was also observed after injection of MethA tumor, DH-5alpha cells, and leishmania parasites, in addition to AK-5 tumor cells. Cellular migration is mediated by several chemokines and cytokines that also induce heavy influx of immune cells into the peritoneum. MIP-3beta secreted by the mesothelial cells is involved in the cellular influx into the peritoneum, whereas IL-12 and IFN-gamma produced by the APCs induced activation of immune cells in the peritoneum. Our results suggest an antigen presentation function for the APCs in the peritoneum as studied by lymphoproliferation assays. These studies indicate antigen presentation function of the activated migratory APCs from the distant subcutaneous site to the peritoneum, suggesting it acts as an important lymphoid organ involved in the enhancement of effector cell function.

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