Histocompatibility Antigens on Murine Tumors

Abstract

Recent advances in tumor immunology suggest that the expression of the histocompatibility antigens, encoded by the major histocompatibility complex, is important in controlling the metastatic growth of certain murine tumors. The anomalous expression of histocompatibility antigens in many neoplasms appears to be associated with the ability of these cells to evade the immune system and progress to metastasis. This review examines some of the underlying molecular and immunobiological interactions that might determine the metastatic outcome of cellular transformation.

Concurrent infiltration by CD8+ T cells and CD4+ T cells is a favourable prognostic factor in non-small-cell lung carcinoma

“…The reasons for this discrepancy were difficult to explain, because the antitumour effect of CD8 þ T cells may be circumvented by various mechanisms in the tumour cells. Tumour cells may obtain the ability to evade immune surveillance by several strategies, including a lack of adequate T-cell costimulation (Melero et al, 1997;Thomas et al, 1999), downregulation of cell-surface MHC class I expression (Goodenow et al, 1985;Restifo et al, 1993;Imboden et al, 2001), dysfunction of Fas (CD95/APO1)-mediated apoptosis (Hahne et al, 1996;Strand et al, 1996) and secretion of immunosuppressive factors, such as transforming growth factor-b (Inge et al, 1992) or interleukin-10 (Fiorentino et al, 1991a, b). Thus, the efficiency of the immune reaction against cancers can be evaded by a variety of mechanisms used by tumour cells, and these can vary, depending on the individual cancer.…”

Instability of expression of major histocompatibility antigens in fibroblasts expressing activated ras oncogene: constitutive and interferon-gamma induced class I and class II antigens in a series of clonal isolates of murine fibroblasts transformed by v-Ki-ras

“…There is accumulating evidence that (at least in experimental systems) the ability of a tumour to grow in a syngeneic host is governed by the density of major histocompatibility complex (MHC) antigens on the surface of the tumour cell (Goodenow et al, 1985). This is reflected in the finding, for example, that transfecting MHC antigen genes into an MHC antigen negative tumour line (so that it becomes antigen positive) drastically reduces its tumorigenicity (Hui et al, 1984;Tanaka et al, 1985;Wallich et al, 1985).…”

A phase I trial of immunotherapy with intratumoral adenovirus-interferon-gamma (TG1041) in patients with malignant melanoma

“…[2][3][4][5] IFN-g treatment of various nonantigenic tumors has been demonstrated to make them highly antigenic, and this correlates with an increase in expression levels of IFN-g-inducible genes that regulate MHC class I presentation. 6,7 IFN-g is capable of upregulating the expression of tumor-associated antigens in vitro and in vivo, [8][9][10] thereby increasing the susceptibility of tumors to MHC-restricted CD8+ cytotoxic Tcell-mediated lysis. IFN-g also activates macrophages to nonspecifically lyse neoplastic cells through various mechanisms.…”