Tumour surveillance: Missing peptides and MHC molecules

Immunotherapy involving CTL is an attractive alternative for treatment of various malignancies. One of the approaches currently being explored for immune targeting of human cancers involves potentiation of immunogenicity of malignant cells by gene transduction. This strategy is undoubtedly influenced by the ability of the malignant cells to endogenously process and present target epitopes on their cell surface for immune recognition by CTL. However, there is increasing evidence to suggest that a large proportion of human cancers escape CTL‐mediated immune surveillance by selectively down‐regulating the expression of MHC class I molecules and peptide transporter genes. Understanding and molecular analysis of these immunologically relevant genetic defects in tumours is very important before translating preclinical studies of immunotherapy to rational clinical trials. Careful consideration of these potential limitations may lead to the development of novel immunotherapeutic strategies and, potentially, prevention of tumour progression or development.

[1]  P. Chomez,et al.  A gene encoding an antigen recognized by cytolytic T lymphocytes on a human melanoma. , 1991, Science.

[2]  F. Marincola,et al.  Loss of HLA haplotype and B locus down-regulation in melanoma cell lines. , 1994, Journal of immunology.

[3]  R. Doms,et al.  Regulation of protein export from the endoplasmic reticulum. , 1988, Annual review of cell biology.

[4]  R. Tampé,et al.  Expression and function of the peptide transporters in escape variants of human renal cell carcinomas. , 1997, Experimental hematology.

[5]  P. Kloetzel,et al.  LMP-associated proteolytic activities and TAP-dependent peptide transport for class 1 MHC molecules are suppressed in cell lines transformed by the highly oncogenic adenovirus 12 , 1996, The Journal of experimental medicine.

[6]  S. Beck,et al.  Sequences encoded in the class II region of the MHC related to the 'ABC' superfamily of transporters , 1990, Nature.

[7]  T. Schumacher,et al.  Transporters from H-2b, H-2d, H-2s, H-2k, and H-2g7 (NOD/Lt) haplotype translocate similar sets of peptides. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[8]  S. Steinberg,et al.  Combination therapy with interleukin-2 and alpha-interferon for the treatment of patients with advanced cancer. , 1989, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[9]  S. Rosenberg,et al.  Human CD4+ T cells specifically recognize a shared melanoma-associated antigen encoded by the tyrosinase gene. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[10]  J. Yewdell,et al.  Trimming of antigenic peptides in an early secretory compartment , 1994, The Journal of experimental medicine.

[11]  P. Robbins,et al.  Human tumor antigens recognized by T cells. , 1996, Current opinion in immunology.

[12]  B. Walker,et al.  Presentation of endogenous peptides to MHC class I-restricted cytotoxic T lymphocytes in transport deletion mutant T2 cells. , 1993, Journal of immunology.

[13]  S. Rosenberg,et al.  Synthetic oligonucleotide expressed by a recombinant vaccinia virus elicits therapeutic CTL. , 1995, Journal of immunology.

[14]  R. Tampé,et al.  A critical role for tapasin in the assembly and function of multimeric MHC class I-TAP complexes. , 1997, Science.

[15]  S. Rosenberg,et al.  Therapeutic antitumor response after immunization with a recombinant adenovirus encoding a model tumor-associated antigen. , 1996, Journal of immunology.

[16]  M. Carrington,et al.  Expression of HLA class I molecules and the transporter associated with antigen processing in hepatocellular carcinoma , 1996, Hepatology.

[17]  C. Slingluff,et al.  The role of HLA class I antigens in recognition of melanoma cells by tumor-specific cytotoxic T lymphocytes. Evidence for shared tumor antigens. , 1989, Journal of immunology.

[18]  D J Moss,et al.  Peptide transporter (TAP-1 and TAP-2)-independent endogenous processing of Epstein-Barr virus (EBV) latent membrane protein 2A: implications for cytotoxic T-lymphocyte control of EBV-associated malignancies , 1996, Journal of virology.

[19]  A. Goldberg Functions of the proteasome: the lysis at the end of the tunnel. , 1995, Science.

[20]  C. Meijer,et al.  Differences in MHC and TAP-1 expression in cervical cancer lymph node metastases as compared with the primary tumours. , 1994, British Journal of Cancer.

[21]  S. Rosenberg,et al.  Quantitative correlation between HLA class I allele expression and recognition of melanoma cells by antigen-specific cytotoxic T lymphocytes. , 1995, Cancer research.

[22]  G. Klein,et al.  aberrant expression of HLA Class‐I antigens in burkitt lymphoma cells , 1991, International journal of cancer.

[23]  P M Kloetzel,et al.  Peptide antigen production by the proteasome: complexity provides efficiency. , 1996, Immunology today.

[24]  P. Coulie,et al.  A mutated intron sequence codes for an antigenic peptide recognized by cytolytic T lymphocytes on a human melanoma. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[25]  A. Harris,et al.  Loss of transporter in antigen processing 1 transport protein and major histocompatibility complex class I molecules in metastatic versus primary breast cancer. , 1995, Cancer research.

[26]  R. Tampé,et al.  Analysis of the major histocompatibility complex class I antigen presentation machinery in normal and malignant renal cells: evidence for deficiencies associated with transformation and progression. , 1996, Cancer research.

[27]  P. Romero,et al.  Human gene MAGE-3 codes for an antigen recognized on a melanoma by autologous cytolytic T lymphocytes , 1994, The Journal of experimental medicine.

[28]  S. Burrows,et al.  Endoplasmic reticulum signal sequence facilitated transport of peptide epitopes restores immunogenicity of an antigen processing defective tumour cell line. , 1994, International immunology.

[29]  J. Neefjes,et al.  Trimming of TAP-translocated peptides in the endoplasmic reticulum and in the cytosol during recycling , 1994, The Journal of experimental medicine.

[30]  S. Burrows,et al.  Engagement of CD40 antigen with soluble CD40 ligand up-regulates peptide transporter expression and restores endogenous processing function in Burkitt's lymphoma cells. , 1997, Journal of immunology.

[31]  S. Ferrone,et al.  Differential expression of melanoma associated antigens in acral lentiginous melanoma and in nodular melanoma lesions. , 1991, Cancer research.

[32]  C. Meijer,et al.  Loss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas , 1994, The Journal of experimental medicine.

[33]  R. Tampé,et al.  Constitutive transduction of peptide transporter and HLA genes restores antigen processing function and cytotoxic T cell‐mediated immune recognition of human melanoma cells , 1998, International journal of cancer.

[34]  R. Siliciano,et al.  An epitope-selective, transporter associated with antigen presentation (TAP)-1/2-independent pathway and a more general TAP-1/2-dependent antigen-processing pathway allow recognition of the HIV-1 envelope glycoprotein by CD8+ CTL. , 1995, Journal of immunology.

[35]  J. Trowsdale,et al.  Restoration of endogenous antigen processing in Burkitt's lymphoma cells by Epstein‐Barr virus latent membrane protein‐1: coordinate up‐regulation of peptide transporters and HLA‐class I antigen expression , 1995, European journal of immunology.

[36]  R. Linsk,et al.  Histocompatibility antigens on murine tumors. , 1985, Science.

[37]  J. Bryant,et al.  Tumor escape from immune recognition: lethal recurrent melanoma in a patient associated with downregulation of the peptide transporter protein TAP-1 and loss of expression of the immunodominant MART-1/Melan-A antigen. , 1996, The Journal of clinical investigation.

[38]  P. Cresswell,et al.  Class I processing-defective Burkitt's lymphoma cells are recognized efficiently by CD4+ EBV-specific CTLs. , 1997, Journal of immunology.

[39]  M. Sanda,et al.  Molecular characterization of defective antigen processing in human prostate cancer. , 1995, Journal of the National Cancer Institute.

[40]  R. Tampé,et al.  A sequential model for peptide binding and transport by the transporters associated with antigen processing. , 1994, Immunity.

[41]  S. Rosenberg,et al.  Melanoma‐specific CD4+ T lymphocytes recognize human melanoma antigens processed and presented by epstein‐barr virus‐transformed B cells , 1994, International journal of cancer.

[42]  R. Brasseur,et al.  BAGE: a new gene encoding an antigen recognized on human melanomas by cytolytic T lymphocytes. , 1995, Immunity.

[43]  H. Rammensee,et al.  Isolation of naturally processed peptides recognized by cytolytic T lymphocytes (CTL) on human melanoma cells in association with HLA‐A2.1 , 1994, International journal of cancer.

[44]  R. Henderson,et al.  HLA-A2.1-associated peptides from a mutant cell line: a second pathway of antigen presentation. , 1992, Science.

[45]  J. Yewdell,et al.  Identification of human cancers deficient in antigen processing , 1993, The Journal of experimental medicine.

[46]  W. Bodmer,et al.  MHC antigens and cancer: Implications for T-cell surveillance , 1992, Current Biology.

[47]  F. Marincola,et al.  Loss of HLA class I antigens by melanoma cells: molecular mechanisms, functional significance and clinical relevance. , 1995, Immunology today.

[48]  R. Demars,et al.  A gene in the human major histocompatibility complex class II region controlling the class I antigen presentation pathway , 1990, Nature.

[49]  A. Harris,et al.  Loss of major histocompatibility complex-encoded transporter associated with antigen presentation (TAP) in colorectal cancer. , 1994, The American journal of pathology.

[50]  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.

[51]  Maria L. Wei,et al.  HLA-A2 molecules in an antigen-processing mutant cell contain signal sequence-derived peptides , 1992, Nature.

[52]  R. Siliciano,et al.  Transporter-independent processing of HIV-1 envelope protein for recognition by CD8+ T cells , 1993, Nature.

[53]  P. Greenberg,et al.  Requirement for recognition of class II molecules and processed tumor antigen for optimal generation of syngeneic tumor-specific class I-restricted CTL. , 1986, Journal of immunology.