HLA-G and IL-10 expression in human cancer--different stories with the same message.

Immune evasion in cancer may result from structural and functional alterations of human leukocyte antigen (HLA) class I molecules and/or local release of immunosuppressive cytokines, such as interleukin (IL)-10. In lung cancer, both of these mechanisms seem to often take place, resulting in the impaired tumor recognition and the progression of the disease. In primary cutaneous lymphomas on the other side, the shift towards immunosuppressive T helper (Th)2 cytokine profile and the secretion of IL-10 appears to occur more frequently than the loss of HLA class I molecules. In addition to down-regulation of HLA class I expression, IL-IO appears to be one of the factors responsible for the up-regulation of HLA-G, another molecule involved in the immunescape. It is possible that the expression of HLA-G itself may account for induction of Th2-skewing state and the production of IL-10, thence establishing a vicious circle of immune abrogation in cancer. This article reviews the current literature on this topic and provides new insights into the role of HLA-G and IL-10 in cancer.