T cell defined tumor antigens

Current Opinion in Immunology

Volumn 9, Issue 5, 1997, Pages 684-693

  Van Den Eynde, Benoît J ^a   Van Der Bruggen, Pierre ^a  

^a LUDWIG INSTITUTE FOR CANCER RESEARCH   (Belgium)

Author keywords

[No Author keywords available]

Indexed keywords

DIFFERENTIATION ANTIGEN; TUMOR ANTIGEN;

ANTIGEN EXPRESSION; CARCINOGENESIS; MUTATION; REVIEW; T LYMPHOCYTE;

EID: 0030696676     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(97)80050-7     Document Type: Article

References (106)

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41. Rubinfeld B, Robbins P, El-Gamil M, Albert I, Porfiri E, Polakis P. Stabilization of β-catenin by genetic defects in melanoma cell lines. of outstanding interest Science. 275:1997;1790-1792 β-catenin was previously found to be mutated at Ser47 in a melanoma cell line, and a peptide corresponding to this mutation was recognized by autologous CTLs [40]. In this paper, the same mutation is found in three out of seven other melanoma lines. β-catenin is implicated in signal transduction (reviewed in [42]) and it combines with the transcription factors Lef and TCF to activate transcription of target genes. Ser47 appears to be necessary for the rapid degradation of β-catenin. When mutated at this residue, β-catenin is stabilized and constitutively forms activating complexes with Lef and TCF. The inappropriate gene activation that results may play a role in melanoma oncogenesis or progression. Interestingly, the responsible DNA mutation is often a C→T transition that may result from ultraviolet radiation of the DNA.
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50. + T cell line proliferated when stimulated either with HLA-DR4 positive cells pulsed with the peptide or with HLA-DR4 positive b3a2-positive leukemic blasts.
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55. Lustgarten J, Theobald M, Labadie C, LaFace D, Peterson P, Disis ML, Cheever MA, Sherman LA. Identification of Her-2/neu CTL epitopes using double transgenic mice expressing HLA-A2.1 and human CD.8. of special interest Hum Immunol. 52:1997;109-118 The HER-2/neu peptide described in [54] and a second HER-2/neu peptide were found to activate CTLs in double transgenic mice expressing both human CD8 and HLA-A2.1 molecules. These mice provide an interesting alternative approach for identifying human T cell epitopes. Recognition of these epitopes by human CTLs will need to be tested, however, because mouse and human T cell repertoires may differ.
56. Röpke M, Hald J, Guldberg P, Zeuthen J, Norgaard L, Fugger L, Svejgaard A, Van Der Burg S, Nijman HW, Melief CJM, Claesson MH. Spontaneous human squamous cell carcinomas are killed by a human cytotoxic T lymphocyte clone recognizing a wild-type p53-derived peptide. of special interest Proc Natl Acad Sci USA. 93:1996;14704-14707 A peptide corresponding to a segment of the wild-type sequence of p53 was used to stimulate blood lymphocytes derived from an HLA-A2 individual. A CTL clone was obtained that lysed an HLA-A2 tumor line that overexpresses p53 due to a mutation located in another part of the sequence. It is not yet clear whether this recognition is related only to p53 overexpression, as one of the three other tumor lines that did not overexpress p53 was also recognized by the CTLs.
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64. Hsu FJ, Caspar CB, Czerwinski D, Kwak LW, Liles TM, Syrengelas A, Taidi-Laskowski B, Levy R. Tumor-specific idiotype vaccines in the treatment of patients with B-cell lymphoma. Long-term results of a clinical trial. of special interest Blood. 89:1997;3129-3135 In this clinical trial, 41 B cell lymphoma patients were immunized with the recombinant idiotypic immunoglobulin derived from their tumor, coupled to key-hole limpet hemocyanin and mixed with adjuvant. About 50% of the patients developed immune responses, as evaluated by the induction of idiotype-specific antibodies and specific T cell proliferation responses. These patients enjoyed improved clinical outcomes as compared with those who did not respond immunologically. 2 of the 20 tumor-bearing patients experienced complete regression in association with the development of these immune responses. In a pilot study by this group [65], the idiotypic protein was used to pulse ex vivo dendritic cells that were then reinjected as a vaccine. T cell responses and tumor regressions were observed in a few patients.
65. Hsu FJ, Benike C, Fagnoni F, Liles TM, Czerwinski D, Taidi B, Engleman EG, Levy R. Vaccination of patients with B-cell lymphoma using autologous antigen-pulsed dendritic cells. Nat Med. 2:1996;52-58.
66. Nelson EL, Li X, Hsu FJ, Kwak LW, Levy R, Clayberger C, Krensky AM. Tumor-specific, cytotoxic T-lymphocyte response after idiotype vaccination for B-cell, non-Hogkin's lymphoma. of special interest Blood. 88:1996;580-589 The same trial as [64], but here a subset of patients were tested for CTL responses. Tumor-specific CTL precursor (CTLp) frequencies were measured by limiting dilution assays before and after treatment. Increases in CTLp frequency were observed in 11 out of 16 patients and they tended to correlate with a better clinical evolution.
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71. PMEL17 (two peptides). Four cycles of weekly injections were performed four weeks apart, and granulocyte-macrophage colony-stimulating factor was injected systemically during the last cycle. Delayed-type hypersensitivity reactions and peptide-specific CTL responses were elicited in all patients by the tyrosinase peptide (amino acids 1-9), in one patient by the Melan-A peptide (amino acids 26-35), and in one patient by the tyrosinase peptide (amino acids 369-377). Interestingly, vitiligo was observed in two patients and objective tumor regressions in all three patients.
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74. Garrido F, Ruiz-Cabello F, Cabrera T, Perez-Villar JJ, Lopez-Botet M, Duggan-Keen M, Stern PL. Implications for immunosurveillance of altered HLA class I phenotypes in human tumors. Immunol Today. 18:1997;89-95.
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76. Traversari C, van der Bruggen P, Luescher IF, Lurquin C, Chomez P, Van Pel A, De Plaen E, Amar-Costesec A, Boon T. A nonapeptide encoded by human gene MAGE-1 is recognized on HLA-A1 by cytolytic T lymphocytes directed against tumor antigen MZ2-E. J Exp Med. 176:1992;1453-1457.
77. van der Bruggen P, Szikora J-P, Bol P, Wildmann C, Somville M, Sensi M, Boon T. Autologous cytolytic T lymphocytes recognize a MAGE-1 nonapeptide on melanomas expressing HLA-Cw*1601. Eur J Immunol. 24:1994;2134-2140.
78. Gaugler B, Van den Eynde B, van der Bruggen P, Romero P, Gaforio JJ, De Plaen E, Lethé B, Brasseur F, Boon T. Human gene MAGE-3 codes for an antigen recognized on a melanoma by autologous cytolytic T lymphocytes. J Exp Med. 179:1994;921-930.
79. van der Bruggen P, Bastin J, Gajewski T, Coulie PG, Bol P, De Smet C, Traversari C, Townsend A, Boon T. A peptide encoded by human gene MAGE-3 and presented by HLA-A2 induces cytolytic T lymphocytes that recognize tumor cells expressing MAGE-3. Eur J Immunol. 24:1994;3038-3043.
80. Herman J, van der Bruggen P, Luescher I, Mandruzzato S, Romero P, Thonnard J, Fleischhauer K, Boon T, Coulie PG. A peptide encoded by human gene MAGE-3 and presented by HLA-B44 induces cytolytic T lymphocytes that recognize tumor cells expressing MAGE-3. Immunogenetics. 43:1996;377-383.
81. Boël P, Wildmann C, Sensi M-L, Brasseur R, Renauld J-C, Coulie P, Boon T, van der Bruggen P. BAGE, a new gene encoding an antigen recognized on human melanomas by cytolytic T lymphocytes. Immunity. 2:1995;167-175.
82. Van den Eynde B, Peeters O, De Backer O, Gaugler B, Lucas S, Boon T. A new family of genes coding for an antigen recognized by autologous cytolytic T lymphocytes on a human melanoma. J Exp Med. 182:1995;689-698.
83. Guilloux Y, Lucas S, Brichard VG, Van Pel A, Viret C, De Plaen E, Brasseur F, Lethé B, Jotereau F, Boon T. A peptide recognized by human cytolytic T lymphocytes on HLA-A2 melanomas is encoded by an intron sequence of the N-acetylglucosaminyltransferase V gene. J Exp Med. 183:1996;1173-1183.
84. Bloom MB, Perry-Lalley D, Robbins PF, Li Y, El-Gamil M, Rosenberg SA, Yang JC. Identification of tyrosinase-related protein 2 as a tumor rejection antigen for the B16 melanoma. of special interest J Exp Med. 185:1997;453-460 The question of the safety of active human immunotherapy targeted against melanocyte differentiation antigens in the treatment of melanoma is open, due to the potential toxicity towards retina melanocytes. Ideally, this issue should have been addressed in a preclinical animal model, but such a model was not previously available because no corresponding melanoma antigen had been identified in animals. The authors here identified a mouse melanoma antigen recognized by CTLs as a peptide from tyrosinase-related protein-2 (TRP-2), a protein also expressed in melanocytes. In humans also, a peptide from TRP-2 is recognized by CTLs on melanoma [95]. This mouse model antigen will be very useful to assess the potential autoimmune side-effects of specific immunization against melanocyte differentiation antigens.
85. Wölfel T, Van Pel A, Brichard V, Schneider J, Seliger B, Meyer zum Büschenfelde K-H, Boon T. Two tyrosinase nonapeptides recognized on HLA-A2 melanomas by autologous cytolytic T lymphocytes. Eur J Immunol. 24:1994;759-764.
86. Kang X, Kawakami Y, El-Gamil M, Wang R, Sakaguchi K, Yannelli JR, Appella E, Rosenberg SA, Robbins PF. Identification of a tyrosinase epitope recognized by HLA-A24-restricted, tumor-infiltrating lymphocytes. J Immunol. 155:1995;1343-1348.
87. Brichard VG, Herman J, Van Pel A, Wildmann C, Gaugler B, Wölfel T, Boon T, Lethé B. A tyrosinase nonapeptide presented by HLA-B44 is recognized on a human melanoma by autologous cytolytic T lymphocytes. Eur J Immunol. 26:1996;224-230.
88. Kawakami Y, Eliyahu S, Jennings C, Sakaguchi K, Kang X, Southwood S, Robbins PF, Sette A, Appella E, Rosenberg SA. Recognition of multiple epitopes in the human melanoma antigen gp100 by tumor-infiltrating T lymphocytes associated with in vivo tumor regression. J Immunol. 154:1995;3961-3968.
89. Bakker A, Schreurs M, Tafazzul G, De Boer A, Kawakami Y, Adema G, Figdor C. Identification of a novel peptide derived from the melanocyte-specific gp100 antigen as the dominant epitope recognized by an HLA-A2.1-restricted anti-melanoma CTL line. Int J Cancer. 62:1995;97-102.
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91. Kawakami Y, Eliyahu S, Delgado CH, Robbins PF, Sakaguchi K, Appella E, Yannelli JR, Adema GJ, Miki T, Rosenberg SA. Identification of a human melanoma antigen recognized by tumor-infiltrating lymphocytes associated with in vivo tumor rejection. Proc Natl Acad Sci USA. 91:1994;6458-6462.
92. Skipper JCA, Kittlesen DJ, Hendrickson RC, Deacon DD, Harthun NL, Wagner SN, Hunt DF, Engelhard VH, Slingluff CLJ. Shared epitopes for HLA-A3-restricted melanoma-reactive human CTL include a naturally processed epitope from Pmel-17/gp100. J Immunol. 157:1996;5027-5033.
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96. + targets, confirming the involvement of the PSA peptides in LNCaP recognition. Such prostate-specific antigens might be useful for T cell immunotherapy, particularly in patients who have undergone prostatectomy, where the only PSA-expressing cells would be in the metastatic deposits.
97. Mandelboim O, Berke G, Fridkin M, Feldman M, Eisenstein M, Eisenbach L. CTL induction by a tumour-associated antigen octapeptide derived from a murine lung carcinoma. Nature. 369:1994;67-71.
98. Monach PA, Meredith SC, Siegel CT, Schreiber H. A unique tumor antigen produced by a single amino acid substitution. Immunity. 2:1995;45-59.
99. De Bergeyck V, De Plaen E, Chomez P, Boon T, Van Pel A. An intracisternal A particle sequence codes for an antigen recognized by syngeneic cytolytic T lymphocytes on a mouse spontaneous leukemia. Eur J Immunol. 24:1994;2203-2212.
100. Huang AYC, Gulden PH, Woods AS, Thomas MC, Tong CD, Wang W, Engelhard VH, Pasternack G, Cotter R, Hunt D, et al. The immunodominant major histocompatibility complex class I-restricted antigen of a murine colon tumor derives from an endogenous retroviral gene products. of special interest Proc Natl Acad Sci USA. 93:1996;9730-9735 Characterization of the major rejection antigen of the carcinogen-induced murine colon tumor CT26 by the peptide elution approach. The peptide is found to be derived from the envelope protein of an endogenous murine leukemia virus. This env gene is not transcribed in normal tissues. The mechanism of its activation in tumor cells is not defined, but it might be related to a retrotranspositional event as observed in [99]. For this
101. + T lymphocytes against tumor cells bearing mutated epitopes of K-ras p21. Eur J Immunol. 25:1995;2588-2597.
102. Dubey P, Hendrickson RC, Meredith SC, Siegel CT, Shabanowitz J, Skipper JCA, Engelhard VH, Hunt DF, Schreiber H. The immunodominant antigen of an ultraviolet-induced regressor tumor is generated by a sometic point mutation in the DEAD box helicase p68. of special interest J Exp Med. 185:1997;695-705 Identification by the peptide elution approach of the immunodominant antigen of a murine UV-induced tumor. The expression of the antigenic peptide results from a unique mutation in an RNA-helicase called p68. The authors suggest a possible involvement of this mutation in oncogenesis.
103. Uenaka A, Ono T, Akisawa T, Wada H, Yasuda T, Nakayama E. Identification of a unique antigen peptide pRL1 on BALB/c RL1 leukemia recognized by cytotoxic T lymphocytes and its relation to the akt oncogene. J Exp Med. 180:1994;1599-1607.
104. Wada H, Matsuo M, Uenaka A, Shimbara N, Shimizu K, Nakayama E. Rejection antigen peptides on BALB/c RL1 leukemia recognized by cytotoxic T lymphocytes: derivation from the normally untranslated 5′ region of the c-akt proto-oncogene activated by long terminal repeat. Cancer Res. 55:1995;4780-4783.
105. Coulie PG, Lehmann F, Lethé B, Herman J, Lurquin C, Andrawiss M, Boon T. A mutated intron sequence codes for an antigenic peptide recognized by cytolytic T lymphocytes on a human melanoma. Proc Natl Acad Sci USA. 92:1995;7976-7980.
106. Brändle D, Brasseur F, Weynants P, Boon T, Van den Eynde B. A mutated HLA-A2 molecule recognized by autologous cytotoxic T lymphocytes on a human renal cell carcinoma. of special interest J Exp Med. 183:1996;2501-2508 This antigen is unique to this human renal cell carcinoma and results from a point mutation in the HLA-A2 gene. The altered HLA-A2 molecule is recognized by CTLs as an allogeneic HLA molecule. This recognition is apparently independent of the presence of a peptide in the HLA peptide binding groove.