The immune system in patients detects and eliminates tumor cells, but tumors still progress persistently. The mechanisms by which tumor cells survive under the pressure of immune surveillance are not fully understood. This review is to present the evidence from clinical studies, showing a significant correlation of clinicopathological features of carcinoma with: (1) the loss of classical human leukocyte antigen class I, (2) the up-regulation of non-classical human leukocyte antigen class I, pro-apoptotic Fas ligand and receptor-binding cancer antigen expressed on SiSo cells I, and (3) the formation of immunosuppressive microenvironment by up-regulation of transforming growth factor-beta, Galectin-1, inhibitory ligand B7s, indoleamine 2,3-dioxygenase and arginase, as well as by recruitment of tumor-induced myeloid-derived suppressor cells and regulatory T cells. All of these factors may together protect carcinoma cells from the immune-cytotoxicity.
Pubmed ID: 21255410 RIS Download
Mesh terms: Animals | Antigens, CD | Antigens, Neoplasm | Arginase | Fas Ligand Protein | Galectin 1 | Humans | Immune Tolerance | Indoleamine-Pyrrole 2,3,-Dioxygenase | Lymphocyte Activation | Lymphocytes, Tumor-Infiltrating | Neoplasms | Severe Combined Immunodeficiency | T-Lymphocytes, Cytotoxic | Transforming Growth Factor beta
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