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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...

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Autores principales: 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.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2003
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.
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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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