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Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10
Human melanoma cells frequently express CC chemokine receptor (CCR)10, a receptor whose ligand (CCL27) is constitutively produced by keratinocytes. Compared with B16 murine melanoma, cells rendered more immunogenic via overexpression of luciferase, B16 cells that overexpressed both luciferase and CC...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2194242/ https://www.ncbi.nlm.nih.gov/pubmed/14581607 http://dx.doi.org/10.1084/jem.20030593 |
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author | Murakami, Takashi Cardones, Adela R. Finkelstein, Steven E. Restifo, Nicholas P. Klaunberg, Brenda A. Nestle, Frank O. Castillo, S. Sianna Dennis, Phillip A. Hwang, Sam T. |
author_facet | Murakami, Takashi Cardones, Adela R. Finkelstein, Steven E. Restifo, Nicholas P. Klaunberg, Brenda A. Nestle, Frank O. Castillo, S. Sianna Dennis, Phillip A. Hwang, Sam T. |
author_sort | Murakami, Takashi |
collection | PubMed |
description | Human melanoma cells frequently express CC chemokine receptor (CCR)10, a receptor whose ligand (CCL27) is constitutively produced by keratinocytes. Compared with B16 murine melanoma, cells rendered more immunogenic via overexpression of luciferase, B16 cells that overexpressed both luciferase and CCR10 resisted host immune responses and readily formed tumors. In vitro, exposure of tumor cells to CCL27 led to rapid activation of Akt, resistance to cell death induced by melanoma antigen-specific cytotoxic T cells, and phosphatidylinositol-3-kinase (PI3K)–dependent protection from apoptosis induced by Fas cross-linking. In vivo, cutaneous injection of neutralizing antibodies to endogenous CCL27 blocked growth of CCR10-expressing melanoma cells. We propose that CCR10 engagement by locally produced CCL27 allows melanoma cells to escape host immune antitumor killing mechanisms (possibly through activation of PI3K/Akt), thereby providing a means for tumor progression. |
format | Text |
id | pubmed-2194242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21942422008-04-11 Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 Murakami, Takashi Cardones, Adela R. Finkelstein, Steven E. Restifo, Nicholas P. Klaunberg, Brenda A. Nestle, Frank O. Castillo, S. Sianna Dennis, Phillip A. Hwang, Sam T. J Exp Med Article Human melanoma cells frequently express CC chemokine receptor (CCR)10, a receptor whose ligand (CCL27) is constitutively produced by keratinocytes. Compared with B16 murine melanoma, cells rendered more immunogenic via overexpression of luciferase, B16 cells that overexpressed both luciferase and CCR10 resisted host immune responses and readily formed tumors. In vitro, exposure of tumor cells to CCL27 led to rapid activation of Akt, resistance to cell death induced by melanoma antigen-specific cytotoxic T cells, and phosphatidylinositol-3-kinase (PI3K)–dependent protection from apoptosis induced by Fas cross-linking. In vivo, cutaneous injection of neutralizing antibodies to endogenous CCL27 blocked growth of CCR10-expressing melanoma cells. We propose that CCR10 engagement by locally produced CCL27 allows melanoma cells to escape host immune antitumor killing mechanisms (possibly through activation of PI3K/Akt), thereby providing a means for tumor progression. The Rockefeller University Press 2003-11-03 /pmc/articles/PMC2194242/ /pubmed/14581607 http://dx.doi.org/10.1084/jem.20030593 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Murakami, Takashi Cardones, Adela R. Finkelstein, Steven E. Restifo, Nicholas P. Klaunberg, Brenda A. Nestle, Frank O. Castillo, S. Sianna Dennis, Phillip A. Hwang, Sam T. Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title | Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title_full | Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title_fullStr | Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title_full_unstemmed | Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title_short | Immune Evasion by Murine Melanoma Mediated through CC Chemokine Receptor-10 |
title_sort | immune evasion by murine melanoma mediated through cc chemokine receptor-10 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2194242/ https://www.ncbi.nlm.nih.gov/pubmed/14581607 http://dx.doi.org/10.1084/jem.20030593 |
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