Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model

Abstract Mechanisms of tumor immune escape are quite diverse and require specific approaches for their exploration in syngeneic tumor models. In several human malignancies, galectin-9 (gal-9) is suspected to contribute to the immune escape. However, in contrast with what has been done for the infilt...

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Autores principales:	Valentin Baloche, Julie Rivière, Thi Bao Tram Tran, Aurore Gelin, Olivia Bawa, Nicolas Signolle, M′Boyba Khadija Diop, Philippe Dessen, Stéphanie Beq, Muriel David, Pierre Busson
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f1c73674a7d746609c3611d3bc2df3af
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spelling	oai:doaj.org-article:f1c73674a7d746609c3611d3bc2df3af2021-12-02T13:20:03ZSerial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model10.1038/s41598-021-84270-12045-2322https://doaj.org/article/f1c73674a7d746609c3611d3bc2df3af2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-84270-1https://doaj.org/toc/2045-2322Abstract Mechanisms of tumor immune escape are quite diverse and require specific approaches for their exploration in syngeneic tumor models. In several human malignancies, galectin-9 (gal-9) is suspected to contribute to the immune escape. However, in contrast with what has been done for the infiltrating cells, the contribution of gal-9 produced by malignant cells has never been demonstrated in an animal model. Therefore, we derived isogenic clones—either positive or negative for gal-9—from the MB49 murine bladder carcinoma cell line. A progressive and consistent reduction of tumor growth was observed when gal-9-KO cells were subjected to serial transplantations into syngeneic mice. In contrast, tumor growth was unaffected during parallel serial transplantations into nude mice, thus linking tumor inhibition to the enhancement of the immune response against gal-9-KO tumors. This stronger immune response was at least in part explained by changing patterns of response to interferon-γ. One consistent change was a more abundant production of CXCL10, a major inflammatory factor whose production is often induced by interferon-γ. Overall, these observations demonstrate for the first time that serial transplantation into syngeneic mice can be a valuable experimental approach for the exploration of novel mechanisms of tumor immune escape.Valentin BalocheJulie RivièreThi Bao Tram TranAurore GelinOlivia BawaNicolas SignolleM′Boyba Khadija DiopPhilippe DessenStéphanie BeqMuriel DavidPierre BussonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-18 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Valentin Baloche Julie Rivière Thi Bao Tram Tran Aurore Gelin Olivia Bawa Nicolas Signolle M′Boyba Khadija Diop Philippe Dessen Stéphanie Beq Muriel David Pierre Busson Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
description	Abstract Mechanisms of tumor immune escape are quite diverse and require specific approaches for their exploration in syngeneic tumor models. In several human malignancies, galectin-9 (gal-9) is suspected to contribute to the immune escape. However, in contrast with what has been done for the infiltrating cells, the contribution of gal-9 produced by malignant cells has never been demonstrated in an animal model. Therefore, we derived isogenic clones—either positive or negative for gal-9—from the MB49 murine bladder carcinoma cell line. A progressive and consistent reduction of tumor growth was observed when gal-9-KO cells were subjected to serial transplantations into syngeneic mice. In contrast, tumor growth was unaffected during parallel serial transplantations into nude mice, thus linking tumor inhibition to the enhancement of the immune response against gal-9-KO tumors. This stronger immune response was at least in part explained by changing patterns of response to interferon-γ. One consistent change was a more abundant production of CXCL10, a major inflammatory factor whose production is often induced by interferon-γ. Overall, these observations demonstrate for the first time that serial transplantation into syngeneic mice can be a valuable experimental approach for the exploration of novel mechanisms of tumor immune escape.
format	article
author	Valentin Baloche Julie Rivière Thi Bao Tram Tran Aurore Gelin Olivia Bawa Nicolas Signolle M′Boyba Khadija Diop Philippe Dessen Stéphanie Beq Muriel David Pierre Busson
author_facet	Valentin Baloche Julie Rivière Thi Bao Tram Tran Aurore Gelin Olivia Bawa Nicolas Signolle M′Boyba Khadija Diop Philippe Dessen Stéphanie Beq Muriel David Pierre Busson
author_sort	Valentin Baloche
title	Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
title_short	Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
title_full	Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
title_fullStr	Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
title_full_unstemmed	Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model
title_sort	serial transplantation unmasks galectin-9 contribution to tumor immune escape in the mb49 murine model
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/f1c73674a7d746609c3611d3bc2df3af
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Serial transplantation unmasks galectin-9 contribution to tumor immune escape in the MB49 murine model

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