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AltraBio is a contract research company specializing in the analysis of biological and medical data using statistical methods and artificial intelligence.
Trusted globally, AltraBio serves as a research and development partner for leading companies and university hospitals across pharmaceuticals, medical devices, diagnostics, and dermato-cosmetics sectors.
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Development of computational tools for data analysis in regional / national / international consortia.
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Hundreds of completed projects
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Regular customers including top 10 pharmas and leaders in cosmetics
Funding
NEWS
October 2024
Collaborative Day of LyonBioPôle
🚀 AltraBio is thrilled to announce our participation in [...]
September 2024
BacSPaD: A Robust Bacterial Strains’ Pathogenicity Resource
🚀 In the framework of the PEST-BIN project, we [...]
May 2024
18th WRIB
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April 2024
CYTO 2024
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LATEST PUBLICATIONS
2015
van Helden, Mary J; Goossens, Steven; Daussy, Cécile; Mathieu, Anne-Laure; Faure, Fabrice; Marçais, Antoine; Vandamme, Niels; Farla, Natalie; Mayol, Katia; Viel, Sébastien; Degouve, Sophie; Debien, Emilie; Seuntjens, Eve; Conidi, Andrea; Chaix, Julie; Mangeot, Philippe; de Bernard, Simon; Buffat, Laurent; Haigh, Jody J; Huylebroeck, Danny; Lambrecht, Bart N; Berx, Geert; Walzer, Thierry
Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection Journal Article
In: J Exp Med, vol. 212, no. 12, pp. 2015–2025, 2015, ISSN: 1540-9538.
@article{pmid26503444,
title = {Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection},
author = {Mary J van Helden and Steven Goossens and Cécile Daussy and Anne-Laure Mathieu and Fabrice Faure and Antoine Marçais and Niels Vandamme and Natalie Farla and Katia Mayol and Sébastien Viel and Sophie Degouve and Emilie Debien and Eve Seuntjens and Andrea Conidi and Julie Chaix and Philippe Mangeot and Simon de Bernard and Laurent Buffat and Jody J Haigh and Danny Huylebroeck and Bart N Lambrecht and Geert Berx and Thierry Walzer},
doi = {10.1084/jem.20150809},
issn = {1540-9538},
year = {2015},
date = {2015-11-01},
urldate = {2015-11-01},
journal = {J Exp Med},
volume = {212},
number = {12},
pages = {2015--2025},
abstract = {Natural killer (NK) cell maturation is a tightly controlled process that endows NK cells with functional competence and the capacity to recognize target cells. Here, we found that the transcription factor (TF) Zeb2 was the most highly induced TF during NK cell maturation. Zeb2 is known to control epithelial to mesenchymal transition, but its role in immune cells is mostly undefined. Targeted deletion of Zeb2 resulted in impaired NK cell maturation, survival, and exit from the bone marrow. NK cell function was preserved, but mice lacking Zeb2 in NK cells were more susceptible to B16 melanoma lung metastases. Reciprocally, ectopic expression of Zeb2 resulted in a higher frequency of mature NK cells in all organs. Moreover, the immature phenotype of Zeb2(-/-) NK cells closely resembled that of Tbx21(-/-) NK cells. This was caused by both a dependence of Zeb2 expression on T-bet and a probable cooperation of these factors in gene regulation. Transgenic expression of Zeb2 in Tbx21(-/-) NK cells partially restored a normal maturation, establishing that timely induction of Zeb2 by T-bet is an essential event during NK cell differentiation. Finally, this novel transcriptional cascade could also operate in human as T-bet and Zeb2 are similarly regulated in mouse and human NK cells.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Natural killer (NK) cell maturation is a tightly controlled process that endows NK cells with functional competence and the capacity to recognize target cells. Here, we found that the transcription factor (TF) Zeb2 was the most highly induced TF during NK cell maturation. Zeb2 is known to control epithelial to mesenchymal transition, but its role in immune cells is mostly undefined. Targeted deletion of Zeb2 resulted in impaired NK cell maturation, survival, and exit from the bone marrow. NK cell function was preserved, but mice lacking Zeb2 in NK cells were more susceptible to B16 melanoma lung metastases. Reciprocally, ectopic expression of Zeb2 resulted in a higher frequency of mature NK cells in all organs. Moreover, the immature phenotype of Zeb2(-/-) NK cells closely resembled that of Tbx21(-/-) NK cells. This was caused by both a dependence of Zeb2 expression on T-bet and a probable cooperation of these factors in gene regulation. Transgenic expression of Zeb2 in Tbx21(-/-) NK cells partially restored a normal maturation, establishing that timely induction of Zeb2 by T-bet is an essential event during NK cell differentiation. Finally, this novel transcriptional cascade could also operate in human as T-bet and Zeb2 are similarly regulated in mouse and human NK cells.
Helden, Mary J; Goossens, Steven; Daussy, Cécile; Mathieu, Anne-Laure; Faure, Fabrice; cais, Antoine Marc; Vandamme, Niels; Farla, Natalie; Mayol, Katia; Viel, Sébastien; Degouve, Sophie; Debien, Emilie; Seuntjens, Eve; Conidi, Andrea; Chaix, Julie; Mangeot, Philippe; Bernard, Simon; Buffat, Laurent; Haigh, Jody J; Huylebroeck, Danny; Lambrecht, Bart N; Berx, Geert; Walzer, Thierry
Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection Journal Article
In: J. Exp. Med., vol. 212, no. 12, pp. 2015–2025, 2015.
@article{Van_Helden2015-zx,
title = {Terminal NK cell maturation is controlled by concerted actions of T-bet and Zeb2 and is essential for melanoma rejection},
author = {Mary J Helden and Steven Goossens and Cécile Daussy and Anne-Laure Mathieu and Fabrice Faure and Antoine Marc cais and Niels Vandamme and Natalie Farla and Katia Mayol and Sébastien Viel and Sophie Degouve and Emilie Debien and Eve Seuntjens and Andrea Conidi and Julie Chaix and Philippe Mangeot and Simon Bernard and Laurent Buffat and Jody J Haigh and Danny Huylebroeck and Bart N Lambrecht and Geert Berx and Thierry Walzer},
doi = {10.1084/jem.20150809},
year = {2015},
date = {2015-11-01},
urldate = {2015-11-01},
journal = {J. Exp. Med.},
volume = {212},
number = {12},
pages = {2015--2025},
publisher = {Rockefeller University Press},
abstract = {Natural killer (NK) cell maturation is a tightly controlled
process that endows NK cells with functional competence and the
capacity to recognize target cells. Here, we found that the
transcription factor (TF) Zeb2 was the most highly induced TF
during NK cell maturation. Zeb2 is known to control epithelial
to mesenchymal transition, but its role in immune cells is
mostly undefined. Targeted deletion of Zeb2 resulted in impaired
NK cell maturation, survival, and exit from the bone marrow. NK
cell function was preserved, but mice lacking Zeb2 in NK cells
were more susceptible to B16 melanoma lung metastases.
Reciprocally, ectopic expression of Zeb2 resulted in a higher
frequency of mature NK cells in all organs. Moreover, the
immature phenotype of Zeb2(-/-) NK cells closely resembled that
of Tbx21(-/-) NK cells. This was caused by both a dependence of
Zeb2 expression on T-bet and a probable cooperation of these
factors in gene regulation. Transgenic expression of Zeb2 in
Tbx21(-/-) NK cells partially restored a normal maturation,
establishing that timely induction of Zeb2 by T-bet is an
essential event during NK cell differentiation. Finally, this
novel transcriptional cascade could also operate in human as
T-bet and Zeb2 are similarly regulated in mouse and human NK
cells.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Natural killer (NK) cell maturation is a tightly controlled
process that endows NK cells with functional competence and the
capacity to recognize target cells. Here, we found that the
transcription factor (TF) Zeb2 was the most highly induced TF
during NK cell maturation. Zeb2 is known to control epithelial
to mesenchymal transition, but its role in immune cells is
mostly undefined. Targeted deletion of Zeb2 resulted in impaired
NK cell maturation, survival, and exit from the bone marrow. NK
cell function was preserved, but mice lacking Zeb2 in NK cells
were more susceptible to B16 melanoma lung metastases.
Reciprocally, ectopic expression of Zeb2 resulted in a higher
frequency of mature NK cells in all organs. Moreover, the
immature phenotype of Zeb2(-/-) NK cells closely resembled that
of Tbx21(-/-) NK cells. This was caused by both a dependence of
Zeb2 expression on T-bet and a probable cooperation of these
factors in gene regulation. Transgenic expression of Zeb2 in
Tbx21(-/-) NK cells partially restored a normal maturation,
establishing that timely induction of Zeb2 by T-bet is an
essential event during NK cell differentiation. Finally, this
novel transcriptional cascade could also operate in human as
T-bet and Zeb2 are similarly regulated in mouse and human NK
cells.
process that endows NK cells with functional competence and the
capacity to recognize target cells. Here, we found that the
transcription factor (TF) Zeb2 was the most highly induced TF
during NK cell maturation. Zeb2 is known to control epithelial
to mesenchymal transition, but its role in immune cells is
mostly undefined. Targeted deletion of Zeb2 resulted in impaired
NK cell maturation, survival, and exit from the bone marrow. NK
cell function was preserved, but mice lacking Zeb2 in NK cells
were more susceptible to B16 melanoma lung metastases.
Reciprocally, ectopic expression of Zeb2 resulted in a higher
frequency of mature NK cells in all organs. Moreover, the
immature phenotype of Zeb2(-/-) NK cells closely resembled that
of Tbx21(-/-) NK cells. This was caused by both a dependence of
Zeb2 expression on T-bet and a probable cooperation of these
factors in gene regulation. Transgenic expression of Zeb2 in
Tbx21(-/-) NK cells partially restored a normal maturation,
establishing that timely induction of Zeb2 by T-bet is an
essential event during NK cell differentiation. Finally, this
novel transcriptional cascade could also operate in human as
T-bet and Zeb2 are similarly regulated in mouse and human NK
cells.
Bauer, Yasmina; Tedrow, John; de Bernard, Simon; Birker-Robaczewska, Magdalena; Gibson, Kevin F; Guardela, Brenda Juan; Hess, Patrick; Klenk, Axel; Lindell, Kathleen O; Poirey, Sylvie; Renault, Bérengère; Rey, Markus; Weber, Edgar; Nayler, Oliver; Kaminski, Naftali
A novel genomic signature with translational significance for human idiopathic pulmonary fibrosis Journal Article
In: Am J Respir Cell Mol Biol, vol. 52, no. 2, pp. 217–231, 2015, ISSN: 1535-4989.
@article{pmid25029475,
title = {A novel genomic signature with translational significance for human idiopathic pulmonary fibrosis},
author = {Yasmina Bauer and John Tedrow and Simon de Bernard and Magdalena Birker-Robaczewska and Kevin F Gibson and Brenda Juan Guardela and Patrick Hess and Axel Klenk and Kathleen O Lindell and Sylvie Poirey and Bérengère Renault and Markus Rey and Edgar Weber and Oliver Nayler and Naftali Kaminski},
doi = {10.1165/rcmb.2013-0310OC},
issn = {1535-4989},
year = {2015},
date = {2015-02-01},
urldate = {2015-02-01},
journal = {Am J Respir Cell Mol Biol},
volume = {52},
number = {2},
pages = {217--231},
abstract = {The bleomycin-induced rodent lung fibrosis model is commonly used to study mechanisms of lung fibrosis and to test potential therapeutic interventions, despite the well recognized dissimilarities to human idiopathic pulmonary fibrosis (IPF). Therefore, in this study, we sought to identify genomic commonalities between the gene expression profiles from 100 IPF lungs and 108 control lungs that were obtained from the Lung Tissue Research Consortium, and rat lungs harvested at Days 3, 7, 14, 21, 28, 42, and 56 after bleomycin instillation. Surprisingly, the highest gene expression similarity between bleomycin-treated rat and IPF lungs was observed at Day 7. At this point of maximal rat-human commonality, we identified a novel set of 12 disease-relevant translational gene markers (C6, CTHRC1, CTSE, FHL2, GAL, GREM1, LCN2, MMP7, NELL1, PCSK1, PLA2G2A, and SLC2A5) that was able to separate almost all patients with IPF from control subjects in our cohort and in two additional IPF/control cohorts (GSE10667 and GSE24206). Furthermore, in combination with diffusing capacity of carbon monoxide measurements, four members of the translational gene marker set contributed to stratify patients with IPF according to disease severity. Significantly, pirfenidone attenuated the expression change of one (CTHRC1) translational gene marker in the bleomycin-induced lung fibrosis model, in transforming growth factor-β1-treated primary human lung fibroblasts and transforming growth factor-β1-treated human epithelial A549 cells. Our results suggest that a strategy focused on rodent model-human disease commonalities may identify genes that could be used to predict the pharmacological impact of therapeutic interventions, and thus facilitate the development of novel treatments for this devastating lung disease.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The bleomycin-induced rodent lung fibrosis model is commonly used to study mechanisms of lung fibrosis and to test potential therapeutic interventions, despite the well recognized dissimilarities to human idiopathic pulmonary fibrosis (IPF). Therefore, in this study, we sought to identify genomic commonalities between the gene expression profiles from 100 IPF lungs and 108 control lungs that were obtained from the Lung Tissue Research Consortium, and rat lungs harvested at Days 3, 7, 14, 21, 28, 42, and 56 after bleomycin instillation. Surprisingly, the highest gene expression similarity between bleomycin-treated rat and IPF lungs was observed at Day 7. At this point of maximal rat-human commonality, we identified a novel set of 12 disease-relevant translational gene markers (C6, CTHRC1, CTSE, FHL2, GAL, GREM1, LCN2, MMP7, NELL1, PCSK1, PLA2G2A, and SLC2A5) that was able to separate almost all patients with IPF from control subjects in our cohort and in two additional IPF/control cohorts (GSE10667 and GSE24206). Furthermore, in combination with diffusing capacity of carbon monoxide measurements, four members of the translational gene marker set contributed to stratify patients with IPF according to disease severity. Significantly, pirfenidone attenuated the expression change of one (CTHRC1) translational gene marker in the bleomycin-induced lung fibrosis model, in transforming growth factor-β1-treated primary human lung fibroblasts and transforming growth factor-β1-treated human epithelial A549 cells. Our results suggest that a strategy focused on rodent model-human disease commonalities may identify genes that could be used to predict the pharmacological impact of therapeutic interventions, and thus facilitate the development of novel treatments for this devastating lung disease.