The overall goal of this project is to investigate the significance of altered expression of histocompatibility antigens on the tumor-host relationship. We propose to pursue ongoing studies demonstrating that antigens coded for by the I-A region of the mouse major histocompatibility complex (MHC) are expressed on proliferating type II pneumocytes in lungs of carcinogen-treated, genetically resistant C3HfB/HeN mice. We wish to determine whether this expression is a secondary consequence of immune recognition and mediated by a specific lymphokine, in particular interleukin-1 (IL-1). We also propose to test for the capacity of syngeneic lymphoid cells to recognize the tumor-associated I-A antigen, the influence of IL-1 on this interaction, and the consequence of this interaction on the generation of non-T-cytotoxic cells. We will use additional monoclonal antibodies, clone T-cell lines and virus-specific cytotoxic T cells to investigate the structurally modified H-2K antigen expressed on the lung tumor 85 and to distinguish the H-2K coded antigens on C3HfB/HeN and C3H/HeN mice. We will induce tumors in genetically resistant and susceptible mouse strains and analyze the tumors for altered expression of MHC-coded antigens. The paucity of HLA antigen expression on human small cell carcinoma cell lines and its reexpression following exposure to interferon will be pursued. (AG)
| Vogel, J M; McMillan, M; Martin, W J et al. (1989) Evidence that derivation of the adenocarcinoma LT85 predated establishment of the H-2km2 mutation in a C3Hf colony of mice. J Immunogenet 16:363-71 |
| Vogel, J M; Davis, A C; McKinney, D M et al. (1988) Molecular characterization of the C3HfB/HeN H-2Kkm2 mutation. Implications for the molecular basis of alloreactivity. J Exp Med 168:1781-800 |
