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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.
How can we work together?
Partnership
Development of computational tools for data analysis in regional / national / international consortia.
Examples of current and completed projects:
Subcontracting
Data analysis for companies and university hospitals.
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Hundreds of completed projects
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Regular customers including top 10 pharmas and leaders in cosmetics
Funding
NEWS
March 2023
Best Biological & Medical Data Analysis Research Company 2023 – Western Europe
We are proud to have been awarded the title [...]
January 2023
XXXI Cosmet’in Lyon Skin Science Days
AltraBio will be present at the XXXI Cosmet'in Lyon Skin [...]
September 2021
CYTO Virtual Interactive Event
Why waste your time analyzing cytometry data manually when gating [...]
August 2021
AltraBio automated gating highlighted by a new publication in Human Vaccines & Immuno therapeutics
Our approach developed for gating automation of cytometry data [...]
LATEST PUBLICATIONS
2016
Bachy, Emmanuel; Urb, Mirjam; Chandra, Shilpi; Robinot, Rémy; Bricard, Gabriel; de Bernard, Simon; Traverse-Glehen, Alexandra; Gazzo, Sophie; Blond, Olivier; Khurana, Archana; Baseggio, Lucile; Heavican, Tayla; Ffrench, Martine; Crispatzu, Giuliano; Mondière, Paul; Schrader, Alexandra; Taillardet, Morgan; Thaunat, Olivier; Martin, Nadine; Dalle, Stéphane; Garff-Tavernier, Magali Le; Salles, Gilles; Lachuer, Joel; Hermine, Olivier; Asnafi, Vahid; Roussel, Mikael; Lamy, Thierry; Herling, Marco; Iqbal, Javeed; Buffat, Laurent; Marche, Patrice N; Gaulard, Philippe; Kronenberg, Mitchell; Defrance, Thierry; Genestier, Laurent
CD1d-restricted peripheral T cell lymphoma in mice and humans Journal Article
In: J Exp Med, vol. 213, no. 5, pp. 841–857, 2016, ISSN: 1540-9538.
@article{pmid27069116,
title = {CD1d-restricted peripheral T cell lymphoma in mice and humans},
author = {Emmanuel Bachy and Mirjam Urb and Shilpi Chandra and Rémy Robinot and Gabriel Bricard and Simon de Bernard and Alexandra Traverse-Glehen and Sophie Gazzo and Olivier Blond and Archana Khurana and Lucile Baseggio and Tayla Heavican and Martine Ffrench and Giuliano Crispatzu and Paul Mondière and Alexandra Schrader and Morgan Taillardet and Olivier Thaunat and Nadine Martin and Stéphane Dalle and Magali Le Garff-Tavernier and Gilles Salles and Joel Lachuer and Olivier Hermine and Vahid Asnafi and Mikael Roussel and Thierry Lamy and Marco Herling and Javeed Iqbal and Laurent Buffat and Patrice N Marche and Philippe Gaulard and Mitchell Kronenberg and Thierry Defrance and Laurent Genestier},
doi = {10.1084/jem.20150794},
issn = {1540-9538},
year = {2016},
date = {2016-05-01},
urldate = {2016-05-01},
journal = {J Exp Med},
volume = {213},
number = {5},
pages = {841--857},
abstract = {Peripheral T cell lymphomas (PTCLs) are a heterogeneous entity of neoplasms with poor prognosis, lack of effective therapies, and a largely unknown pathophysiology. Identifying the mechanism of lymphomagenesis and cell-of-origin from which PTCLs arise is crucial for the development of efficient treatment strategies. In addition to the well-described thymic lymphomas, we found that p53-deficient mice also developed mature PTCLs that did not originate from conventional T cells but from CD1d-restricted NKT cells. PTCLs showed phenotypic features of activated NKT cells, such as PD-1 up-regulation and loss of NK1.1 expression. Injections of heat-killed Streptococcus pneumonia, known to express glycolipid antigens activating NKT cells, increased the incidence of these PTCLs, whereas Escherichia coli injection did not. Gene expression profile analyses indicated a significant down-regulation of genes in the TCR signaling pathway in PTCL, a common feature of chronically activated T cells. Targeting TCR signaling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged mice survival. Importantly, we identified human CD1d-restricted lymphoma cells within Vδ1 TCR-expressing PTCL. These results define a new subtype of PTCL and pave the way for the development of blocking anti-CD1d antibody for therapeutic purposes in humans.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Peripheral T cell lymphomas (PTCLs) are a heterogeneous entity of neoplasms with poor prognosis, lack of effective therapies, and a largely unknown pathophysiology. Identifying the mechanism of lymphomagenesis and cell-of-origin from which PTCLs arise is crucial for the development of efficient treatment strategies. In addition to the well-described thymic lymphomas, we found that p53-deficient mice also developed mature PTCLs that did not originate from conventional T cells but from CD1d-restricted NKT cells. PTCLs showed phenotypic features of activated NKT cells, such as PD-1 up-regulation and loss of NK1.1 expression. Injections of heat-killed Streptococcus pneumonia, known to express glycolipid antigens activating NKT cells, increased the incidence of these PTCLs, whereas Escherichia coli injection did not. Gene expression profile analyses indicated a significant down-regulation of genes in the TCR signaling pathway in PTCL, a common feature of chronically activated T cells. Targeting TCR signaling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged mice survival. Importantly, we identified human CD1d-restricted lymphoma cells within Vδ1 TCR-expressing PTCL. These results define a new subtype of PTCL and pave the way for the development of blocking anti-CD1d antibody for therapeutic purposes in humans.
2015
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.
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.