Figure 2.

Hypothetical complementary mechanisms of early immune surveillance of cancer cells. (a) TGF-β3 has been proposed as an autocrine inhibitor of epididymal epithelial cell growth to limit uncontrolled proliferation. (b) A classical immune response may be set for tumour cells. Modified antigens could be sampled by APCs and presented to effector T cells, inducing a cytotoxic response to epithelial tumour cells. (c) γδ T cells can be directly activated by tumour cells to become cytotoxic and can induce indirect activation of cytotoxic CD8⁺ T cells by upregulating stimulating molecules on the tumour cell surface. γδ T cells can also inhibit angiogenesis. As suggested for the immune response, the epididymal fat pad could participate in the early elimination of cancer cells by the release of such cytotoxic cells as γδ T cells, NK cells and NKT cells. (d) DN T cells can selectively recognize transforming cells and become cytotoxic and suppress them. Ep: epithelium; L: lumen; Int.: interstitium; TJ: tight junction; TGF-β: transforming growth factor-beta; APC: antigen-presenting cell; Ag: antigen; NK: natural killer cell; NKT: natural killer T cell; DNT: double-negative T cell.