Natural variation of the expression of HLA and endogenous antigen modulates CTL recognition in an In vitro melanoma model
Increasing attention has been devoted to elucidating the mechanism of lost or decreased expression of MHC or melanoma‐associated antigens (MAAs), which may lead to tumor escape from immune recognition. Loss of expression of HLA class I or MAA has, as an undisputed consequence, loss of recognition by...
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Published in | International journal of cancer Vol. 80; no. 5; pp. 781 - 790 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
John Wiley & Sons, Inc
01.03.1999
Wiley-Liss |
Subjects | |
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Abstract | Increasing attention has been devoted to elucidating the mechanism of lost or decreased expression of MHC or melanoma‐associated antigens (MAAs), which may lead to tumor escape from immune recognition. Loss of expression of HLA class I or MAA has, as an undisputed consequence, loss of recognition by HLA class I–restricted cytotoxic T cells (CTLs). However, the relevance of down‐regulation remains in question in terms of frequency of occurrence. Moreover the functional significance of epitope down‐regulation, defining the relationship between MHC/epitope density and CTL interactions, is a matter of controversy, particularly with regard to whether the noted variability of expression of MHC/epitope occurs within a range likely to affect target recognition by CTLs. In this study, bulk metastatic melanoma cell lines originated from 25 HLA‐A*0201 patients were analyzed for expression of HLA‐A2 and MAAs. HLA‐A2 expression was heterogeneous and correlated with lysis by CTLs. Sensitivity to lysis was also independently affected by the amount of ligand available for binding at concentrations of 0.001 to 1 mM. Natural expression of MAA was variable, independent from the expression of HLA‐A*0201, and a significant co‐factor determining recognition of melanoma targets. Thus, the naturally occurring variation in the expression of MAA and/or HLA documented by our in vitro results modulates recognition of melanoma targets and may (i) partially explain CTL–target interactions in vitro and (ii) elucidate potential mechanisms for progressive escape of tumor cells from immune recognition in vivo. Int. J. Cancer: 80, 781–790 (1999). © 1999 Wiley‐Liss, Inc. |
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AbstractList | Increasing attention has been devoted to elucidating the mechanism of lost or decreased expression of MHC or melanoma-associated antigens (MAAs), which may lead to tumor escape from immune recognition. Loss of expression of HLA class I or MAA has, as an undisputed consequence, loss of recognition by HLA class I-restricted cytotoxic T cells (CTLs). However, the relevance of down-regulation remains in question in terms of frequency of occurrence. Moreover the functional significance of epitope down-regulation, defining the relationship between MHC/epitope density and CTL interactions, is a matter of controversy, particularly with regard to whether the noted variability of expression of MHC/epitope occurs within a range likely to affect target recognition by CTLs. In this study, bulk metastatic melanoma cell lines originated from 25 HLA-A*0201 patients were analyzed for expression of HLA-A2 and MAAs. HLA-A2 expression was heterogeneous and correlated with lysis by CTLs. Sensitivity to lysis was also independently affected by the amount of ligand available for binding at concentrations of 0.001 to 1 mM. Natural expression of MAA was variable, independent from the expression of HLA-A*0201, and a significant co-factor determining recognition of melanoma targets. Thus, the naturally occurring variation in the expression of MAA and/or HLA documented by our in vitro results modulates recognition of melanoma targets and may (i) partially explain CTL-target interactions in vitro and (ii) elucidate potential mechanisms for progressive escape of tumor cells from immune recognition in vivo. Increasing attention has been devoted to elucidating the mechanism of lost or decreased expression of MHC or melanoma-associated antigens (MAAs), which may lead to tumor escape from immune recognition. Loss of expression of HLA class I or MAA has, as an undisputed consequence, loss of recognition by HLA class I–restricted cytotoxic T cells (CTLs). However, the relevance of down-regulation remains in question in terms of frequency of occurrence. Moreover the functional significance of epitope down-regulation, defining the relationship between MHC/epitope density and CTL interactions, is a matter of controversy, particularly with regard to whether the noted variability of expression of MHC/epitope occurs within a range likely to affect target recognition by CTLs. In this study, bulk metastatic melanoma cell lines originated from 25 HLA-A*0201 patients were analyzed for expression of HLA-A2 and MAAs. HLA-A2 expression was heterogeneous and correlated with lysis by CTLs. Sensitivity to lysis was also independently affected by the amount of ligand available for binding at concentrations of 0.001 to 1 mM. Natural expression of MAA was variable, independent from the expression of HLA-A*0201, and a significant co-factor determining recognition of melanoma targets. Thus, the naturally occurring variation in the expression of MAA and/or HLA documented by our in vitro results modulates recognition of melanoma targets and may (i) partially explain CTL–target interactions in vitro and (ii) elucidate potential mechanisms for progressive escape of tumor cells from immune recognition in vivo . Increasing attention has been devoted to elucidating the mechanism of lost or decreased expression of MHC or melanoma‐associated antigens (MAAs), which may lead to tumor escape from immune recognition. Loss of expression of HLA class I or MAA has, as an undisputed consequence, loss of recognition by HLA class I–restricted cytotoxic T cells (CTLs). However, the relevance of down‐regulation remains in question in terms of frequency of occurrence. Moreover the functional significance of epitope down‐regulation, defining the relationship between MHC/epitope density and CTL interactions, is a matter of controversy, particularly with regard to whether the noted variability of expression of MHC/epitope occurs within a range likely to affect target recognition by CTLs. In this study, bulk metastatic melanoma cell lines originated from 25 HLA‐A*0201 patients were analyzed for expression of HLA‐A2 and MAAs. HLA‐A2 expression was heterogeneous and correlated with lysis by CTLs. Sensitivity to lysis was also independently affected by the amount of ligand available for binding at concentrations of 0.001 to 1 mM. Natural expression of MAA was variable, independent from the expression of HLA‐A*0201, and a significant co‐factor determining recognition of melanoma targets. Thus, the naturally occurring variation in the expression of MAA and/or HLA documented by our in vitro results modulates recognition of melanoma targets and may (i) partially explain CTL–target interactions in vitro and (ii) elucidate potential mechanisms for progressive escape of tumor cells from immune recognition in vivo. Int. J. Cancer: 80, 781–790 (1999). © 1999 Wiley‐Liss, Inc. |
Author | Mixon, Arnold Restifo, Nicholas P. Cormier, Janice N. Bettinotti, Maria P. Marincola, Francesco M. Wunderlich, John Parker, Linda L. Hackett, Julia A. Ferrone, Soldano Panelli, Monica C. |
AuthorAffiliation | 2 HLA Laboratory, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, USA 3 Department of Microbiology and Immunology, New York Medical College, Valhalla, NY, USA 1 Surgery Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD, USA |
AuthorAffiliation_xml | – name: 1 Surgery Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD, USA – name: 2 HLA Laboratory, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, USA – name: 3 Department of Microbiology and Immunology, New York Medical College, Valhalla, NY, USA |
Author_xml | – sequence: 1 givenname: Janice N. surname: Cormier fullname: Cormier, Janice N. – sequence: 2 givenname: Monica C. surname: Panelli fullname: Panelli, Monica C. – sequence: 3 givenname: Julia A. surname: Hackett fullname: Hackett, Julia A. – sequence: 4 givenname: Maria P. surname: Bettinotti fullname: Bettinotti, Maria P. – sequence: 5 givenname: Arnold surname: Mixon fullname: Mixon, Arnold – sequence: 6 givenname: John surname: Wunderlich fullname: Wunderlich, John – sequence: 7 givenname: Linda L. surname: Parker fullname: Parker, Linda L. – sequence: 8 givenname: Nicholas P. surname: Restifo fullname: Restifo, Nicholas P. – sequence: 9 givenname: Soldano surname: Ferrone fullname: Ferrone, Soldano – sequence: 10 givenname: Francesco M. surname: Marincola fullname: Marincola, Francesco M. email: marincola@nih.gov. |
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Keywords | Human HLA-System Immune response Tumor associated antigen Major histocompatibility system Variability Melanoma Cytotoxicity Cellular immunity Tumoral marker Malignant tumor In vitro Established cell line T-Lymphocyte Class I histocompatibility antigen |
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References | 1995; 92 1996; 19 1995; 16 1994; 152 1994; 153 1995; 55 1996b; 19 1997; 89 1997 1997; 18 1996; 4 1995; 154 1997; 3 1998; 75 1996a; 19 1996; 66 1996; 88 |
References_xml | – volume: 153 start-page: 1225 year: 1994 end-page: 1237 article-title: Loss of HLA haplotype and B locus down‐regulation in melanoma cell lines publication-title: J. Immunol – volume: 75 start-page: 517 year: 1998 end-page: 524 article-title: Heterogeneous expression of melanoma‐associated antigens (MAA) and HLA‐A2 in metastatic melanoma publication-title: Int. J. Cancer – volume: 89 start-page: 319 year: 1997 end-page: 321 article-title: Low frequency of ErbB‐2 protooncogene overexpression in human leukocyte antigen A2 positive breast cancer patients publication-title: J. nat. Cancer Inst – volume: 92 start-page: 8125 year: 1995 end-page: 8129 article-title: Immunophenotyping of melanomas for tyrosinase: implications for vaccine development publication-title: Proc. nat. Acad. Sci. USA – volume: 19 start-page: 192 year: 1996a end-page: 205 article-title: Analysis of expression of the melanoma associated antigens MART‐1 and gp100 in metastatic melanoma cell lines and in lesions publication-title: J. Immunother – volume: 16 start-page: 487 year: 1995 end-page: 494 article-title: Loss of HLA class I antigens by melanoma cells: molecular mechanisms, functional significance and clinical relevance publication-title: Immunol. Today – volume: 152 start-page: 2393 year: 1994 end-page: 2400 article-title: Association of HER2/neu expression with sensitivity to tumor‐specific CTL in human ovarian cancer publication-title: J. Immunol – volume: 88 start-page: 100 year: 1996 end-page: 108 article-title: The loss of functional b2‐microglobulin in metastatic melanomas from five patients undergoing immunotherapy publication-title: J. nat. Cancer Inst – volume: 152 start-page: 163 year: 1994 end-page: 175 article-title: Scheme for ranking potential HLA‐A2 binding peptides based on independent binding of individual peptide side‐chains publication-title: J. Immunol – volume: 19 start-page: 375 year: 1996 end-page: 380 article-title: Expression of gp100 in melanoma metastases resected before and after treatment with IFNα and IL‐2 publication-title: J. Immunother – volume: 66 start-page: 470 year: 1996 end-page: 476 article-title: Inverse relationship of melanocyte differentiation antigen expression in melanoma tissues and CD8 cytotoxic T‐cell responses: evidence for immunoselection of antigen‐loss variants publication-title: Int. J. Cancer – year: 1997 – volume: 55 start-page: 3149 year: 1995 end-page: 3157 article-title: Quantitative correlation between HLA class I allele expression and recognition of melanoma cells by antigen specific cytotoxic T lymphocytes publication-title: Cancer Res – volume: 4 start-page: 565 year: 1996 end-page: 571 article-title: Evidence that a single peptide–MHC complex on a target cell can elicit a cytolytic T cell response publication-title: Immunity – volume: 154 start-page: 3961 year: 1995 end-page: 3968 article-title: Recognition of multiple epitopes in the human melanoma antigen gp100 by tumor‐infiltrating T lymphocytes associated with tumor regression publication-title: J. Immunol – volume: 18 start-page: 175 year: 1997 end-page: 182 article-title: Cancer vaccines based on the identification of genesencoding cancer regression antigens publication-title: Immunol. Today – volume: 3 start-page: 37 year: 1997 end-page: 44 article-title: Enhancement of cellular immunity in melanoma patients immunized with a peptide from MART‐1/MelanA publication-title: Cancer J. Sci. Am – volume: 19 start-page: 266 year: 1996b end-page: 277 article-title: Differential anti‐MART‐1/MelanA CTL activity in peripheral blood of HLA‐A2 melanoma patients in comparison to healthy donors: evidence for priming by tumor cells publication-title: J. Immunother – volume: 19 start-page: 357 year: 1996 end-page: 363 article-title: Differences in frequency distribution of HLA‐A2 sub‐types between American and Italian Caucasian melanoma patients: relevance for epitope specific vaccination protocols publication-title: J. Immunother |
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SubjectTerms | Antibodies, Monoclonal Antigens, Neoplasm Biological and medical sciences Breast Neoplasms - pathology Cells, Cultured Cytotoxicity, Immunologic Epitopes - immunology Female Genetic Variation Histocompatibility Antigens Class I - biosynthesis Histocompatibility Antigens Class I - genetics Histocompatibility Testing HLA-A Antigens - genetics Host-tumor relations. Immunology. Biological markers Humans Lymphocytes, Tumor-Infiltrating - immunology Major Histocompatibility Complex Medical sciences Melanoma - immunology Melanoma-Specific Antigens Neoplasm Proteins - genetics T-Lymphocytes, Cytotoxic - immunology Tumor Cells, Cultured Tumors |
Title | Natural variation of the expression of HLA and endogenous antigen modulates CTL recognition in an In vitro melanoma model |
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