T Lymphocytes

The principal mechanism of adaptive tumor immunity is killing of tumor cells by CD8+ CTLs. The ability of CTLs to provide effective anti-tumor immunity in vivo is most clearly seen in animal experiments using carcinogen-induced and DNA virus-induced tumors. As discussed previously, CTLs may perform a surveillance function by recognizing and killing potentially malignant cells that express peptides that are derived from tumor antigens and are presented in association with class I MHC molecules. The role of immune surveillance in preventing common, nonvirally induced tumors remains controversial because the frequency of such tumors in T cell-deficient people is not clearly greater than the frequency in immunocompetent individuals. However, tumor-specific CTLs can be isolated from animals and humans with established tumors, and there is evidence that the prognosis of some types of human tumors is better when more CTLs are present. Furthermore, mononuclear cells derived from the inflammatory infiltrate in human solid tumors, called tumor-infiltrating lymphocytes (TILs), contain CTLs with the capacity to kill the tumor from which they were derived.

CD8+ T cell responses specific for tumor antigens may require cross-presentation of the tumor antigens by dendritic cells. Most tumor cells are not derived from APCs and therefore do not express the costimulators needed to initiate T cell responses or the class II MHC molecules needed to stimulate helper T cells that promote the differentiation of CD8+ T cells. A likely explanation for how T cell responses to tumors are initiated is that tumor cells or their antigens are ingested by host APCs, particularly dendritic cells, and tumor antigens are processed inside the APCs. Peptides derived from these antigens are then displayed bound to class I MHC molecules for recognition by CD8+ T cells. The APCs express costimulators that provide the signals needed for differentiation of CD8+ T cells into anti-tumor CTLs, and the APCs express class II MHC molecules that may present internalized tumor antigens and activate CD4+ helper T cells as well (Fig. 17-4). This process of cross-presentation, or evasion of immune responses by tumors 397

Induction of anti-tumor T cell response (cross-priming)

Tumor antigen

Tumor antigen

Tumor cell

Tumor cell

Tumor cells and antigens ingested by host APCs -►

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