Major histocompatibility complex class II+B7-1+ tumor cells are potent vaccines for stimulating tumor rejection in tumor-bearing mice

Mice carrying large established major histocompatibility complex (MHC) class 1+ sarcoma tumors can be successfully treated by immunization with genetically engineered sarcoma cells transfected with syngeneic MHC class II plus B7-1 genes. This approach is significantly more effective than previously described strategies using cytokine- or B7- transduced tumor cells which are only effective against smaller tumor loads, and which cannot mediate regression of longer-term established tumors. The most efficient tumor rejection occurs if both the class II and B7-1 molecules are coexpressed on the same tumor cell. Immunity induced by immunization with class II+B7-1(+)-transfected sarcoma cells involves CD4+ and CD8+ T cells, suggesting that the increased effectiveness of the transfectants is due to their ability to activate both of these T cell populations.

[1]  Lieping Chen,et al.  Costimulation of tumor-reactive CD4+ and CD8+ T lymphocytes by B7, a natural ligand for CD28, can be used to treat established mouse melanoma. , 1994, Journal of immunology.

[2]  S. Ostrand-Rosenberg,et al.  MHC class II-transfected tumor cells induce long-term tumor-specific immunity in autologous mice. , 1994, Cellular immunology.

[3]  M. Sitkovsky,et al.  Development and antigen specificity of CD8+ cytotoxic T lymphocytes in beta 2-microglobulin-negative, MHC class I-deficient mice in response to immunization with tumor cells. , 1994, Journal of immunology.

[4]  J. Johnston,et al.  Tumor immunogenicity determines the effect of B7 costimulation on T cell-mediated tumor immunity , 1994, The Journal of experimental medicine.

[5]  Simon C Watkins,et al.  Fibroblasts genetically engineered to secrete interleukin 12 can suppress tumor growth and induce antitumor immunity to a murine melanoma in vivo. , 1994, Cancer research.

[6]  S. Ostrand-Rosenberg,et al.  Beta 2M-/- knockout mice contain low levels of CD8+ cytotoxic T lymphocyte that mediate specific tumor rejection. , 1993, Journal of immunology.

[7]  H. Ananthaswamy,et al.  Rejection of K1735 murine melanoma in syngeneic hosts requires expression of MHC class I antigens and either class II antigens or IL-2. , 1993, Journal of immunology.

[8]  G. Freeman,et al.  Constitutive expression of B7 restores immunogenicity of tumor cells expressing truncated major histocompatibility complex class II molecules. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[9]  J. Allison,et al.  CD28-B7 interactions allow the induction of CD8+ cytotoxic T lymphocytes in the absence of exogenous help , 1993, The Journal of experimental medicine.

[10]  E. Jaffee,et al.  Vaccination with irradiated tumor cells engineered to secrete murine granulocyte-macrophage colony-stimulating factor stimulates potent, specific, and long-lasting anti-tumor immunity. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[11]  F. Miller,et al.  Induction of antitumor immunity by interleukin-2 gene-transduced mouse mammary tumor cells versus transduced mammary stromal fibroblasts. , 1993, Journal of the National Cancer Institute.

[12]  E. Gilboa,et al.  Regression of bladder tumors in mice treated with interleukin 2 gene- modified tumor cells [published erratum appears in J Exp Med 1993 Jun 1;177(6):following 1831] , 1993, The Journal of experimental medicine.

[13]  L. Lanier,et al.  Requirements for CD28-dependent T cell-mediated cytotoxicity. , 1993, Journal of immunology.

[14]  J. Allison,et al.  Tumor rejection after direct costimulation of CD8+ T cells by B7-transfected melanoma cells. , 1993, Science.

[15]  P. Linsley,et al.  Costimulation of antitumor immunity by the B7 counterreceptor for the T lymphocyte molecules CD28 and CTLA-4 , 1992, Cell.

[16]  G. Freeman,et al.  Murine B7 antigen provides a sufficient costimulatory signal for antigen-specific and MHC-restricted T cell activation. , 1992, Journal of immunology.

[17]  G. Freeman,et al.  Signalling through the MHC class II cytoplasmic domain is required for antigen presentation and induces B7 expression , 1992, Nature.

[18]  C. Janeway,et al.  Cells that present both specific ligand and costimulatory activity are the most efficient inducers of clonal expansion of normal CD4 T cells. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[19]  D. Pardoll New strategies for active immunotherapy with genetically engineered tumor cells. , 1992, Current opinion in immunology.

[20]  D. Pardoll,et al.  Treatment of established renal cancer by tumor cells engineered to secrete interleukin-4. , 1991, Science.

[21]  S. Ostrand-Rosenberg,et al.  Abrogation of tumorigenicity by MHC class II antigen expression requires the cytoplasmic domain of the class II molecule. , 1991, Journal of immunology.

[22]  Eric O Long,et al.  An endogenous processing pathway in vaccinia virus-infected cells for presentation of cytoplasmic antigens to class II-restricted T cells , 1990, The Journal of experimental medicine.

[23]  S. Ostrand-Rosenberg,et al.  Rejection of mouse sarcoma cells after transfection of MHC class II genes. , 1990, Journal of immunology.

[24]  R. Klausner,et al.  Class II MHC molecules can use the endogenous pathway of antigen presentation , 1990, Nature.

[25]  Eric O Long,et al.  HLA class II-restricted presentation of cytoplasmic measles virus antigens to cytotoxic T cells , 1989, Journal of virology.

[26]  R. Schwartz,et al.  Clonal expansion versus functional clonal inactivation: a costimulatory signalling pathway determines the outcome of T cell antigen receptor occupancy. , 1989, Annual review of immunology.

[27]  P. Marrack,et al.  Evidence implicating L3T4 in class II MHC antigen reactivity; monoclonal antibody GK1.5 (anti-L3T4a) blocks class II MHC antigen-specific proliferation, release of lymphokines, and binding by cloned murine helper T lymphocyte lines. , 1983, Journal of immunology.

[28]  A. Glasebrook,et al.  IgG or IgM monoclonal antibodies reactive with different determinants on the molecular complex bearing Lyt 2 antigen block T cell-mediated cytolysis in the absence of complement. , 1980, Journal of immunology.

[29]  L. Herzenberg,et al.  Properties of monoclonal antibodies to mouse Ig allotypes, H-2, and Ia antigens. , 1978, Current topics in microbiology and immunology.