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AltraBio est une société de recherche contractuelle spécialisée dans l’analyse de données biologiques et médicales grâce à l’utilisation de méthodes statistiques et d’intelligence artificielle.
Elle est reconnue mondialement comme un partenaire de confiance pour les projets de recherche et développement menés par de grandes entreprises et des hôpitaux universitaires de premier plan évoluant dans divers secteurs tels que les produits pharmaceutiques, les dispositifs médicaux, le diagnostic et les dermato-cosmétiques.
COMMENT TRAVAILLER ENSEMBLE?
Partenariat
Développement d’outils informatiques pour l’analyse de données au sein de consortiums régionaux / nationaux / internationaux.
Exemples de projets réalisés ou en cours:
Sous-traitance
Analyse de données pour des entreprises ou des instituts hospitalo-universitaires.
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Des centaines de projets réalisés
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Des clients réguliers incluant les plus grandes pharmas et les leaders de la cosmétique
FINANCEMENTS
NOUVELLES
mai 2024
18e WRIB
🔬 Nous sommes ravis d'annoncer notre participation au 18e [...]
avril 2024
CYTO 2024
🔬 Nous sommes ravis d'annoncer notre participation au congrès [...]
janvier 2024
Colloque I3M
Nous sommes ravis d'annoncer notre présence au prochain colloque [...]
novembre 2023
Immunotherapies & Innovations for Infectious Diseases
AltraBio est ravi d'annoncer sa présence au prochain I4ID Congress [...]
DERNIERES PUBLICATIONS
2016
Brinza, Lilia; Djebali, Sophia; Tomkowiak, Martine; Mafille, Julien; Loiseau, Céline; Jouve, Pierre-Emmanuel; Bernard, Simon; Buffat, Laurent; Lina, Bruno; Ottmann, Mich`ele; Rosa-Calatrava, Manuel; Schicklin, Stéphane; Bonnefoy, Nathalie; Lauvau, Grégoire; Grau, Morgan; Wencker, Mélanie; Arpin, Christophe; Walzer, Thierry; Leverrier, Yann; Marvel, Jacqueline
Immune signatures of protective spleen memory CD8 T cells Article de journal
Dans: Sci. Rep., vol. 6, p. 37651, 2016.
@article{Brinza2016-gb,
title = {Immune signatures of protective spleen memory CD8 T cells},
author = {Lilia Brinza and Sophia Djebali and Martine Tomkowiak and Julien Mafille and Céline Loiseau and Pierre-Emmanuel Jouve and Simon Bernard and Laurent Buffat and Bruno Lina and Mich`ele Ottmann and Manuel Rosa-Calatrava and Stéphane Schicklin and Nathalie Bonnefoy and Grégoire Lauvau and Morgan Grau and Mélanie Wencker and Christophe Arpin and Thierry Walzer and Yann Leverrier and Jacqueline Marvel},
doi = {10.1038/srep37651},
year = {2016},
date = {2016-11-01},
urldate = {2016-11-01},
journal = {Sci. Rep.},
volume = {6},
pages = {37651},
abstract = {Memory CD8 T lymphocyte populations are remarkably heterogeneous
and differ in their ability to protect the host. In order to
identify the whole range of qualities uniquely associated with
protective memory cells we compared the gene expression
signatures of two qualities of memory CD8 T cells sharing the
same antigenic-specificity: protective (Influenza-induced,
Flu-TM) and non-protective (peptide-induced, TIM) spleen memory
CD8 T cells. Although Flu-TM and TIM express classical phenotypic
memory markers and are polyfunctional, only Flu-TM protects
against a lethal viral challenge. Protective memory CD8 T cells
express a unique set of genes involved in migration and survival
that correlate with their unique capacity to rapidly migrate
within the infected lung parenchyma in response to influenza
infection. We also enlighten a new set of poised genes expressed
by protective cells that is strongly enriched in cytokines and
chemokines such as Ccl1, Ccl9 and Gm-csf. CCL1 and GM-CSF genes
are also poised in human memory CD8 T cells. These immune
signatures are also induced by two other pathogens (vaccinia
virus and Listeria monocytogenes). The immune signatures
associated with immune protection were identified on circulating
cells, i.e. those that are easily accessible for
immuno-monitoring and could help predict vaccines efficacy.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
and differ in their ability to protect the host. In order to
identify the whole range of qualities uniquely associated with
protective memory cells we compared the gene expression
signatures of two qualities of memory CD8 T cells sharing the
same antigenic-specificity: protective (Influenza-induced,
Flu-TM) and non-protective (peptide-induced, TIM) spleen memory
CD8 T cells. Although Flu-TM and TIM express classical phenotypic
memory markers and are polyfunctional, only Flu-TM protects
against a lethal viral challenge. Protective memory CD8 T cells
express a unique set of genes involved in migration and survival
that correlate with their unique capacity to rapidly migrate
within the infected lung parenchyma in response to influenza
infection. We also enlighten a new set of poised genes expressed
by protective cells that is strongly enriched in cytokines and
chemokines such as Ccl1, Ccl9 and Gm-csf. CCL1 and GM-CSF genes
are also poised in human memory CD8 T cells. These immune
signatures are also induced by two other pathogens (vaccinia
virus and Listeria monocytogenes). The immune signatures
associated with immune protection were identified on circulating
cells, i.e. those that are easily accessible for
immuno-monitoring and could help predict vaccines efficacy.
Brinza, Lilia; Djebali, Sophia; Tomkowiak, Martine; Mafille, Julien; Loiseau, Céline; Jouve, Pierre-Emmanuel; de Bernard, Simon; Buffat, Laurent; Lina, Bruno; Ottmann, Michèle; Rosa-Calatrava, Manuel; Schicklin, Stéphane; Bonnefoy, Nathalie; Lauvau, Grégoire; Grau, Morgan; Wencker, Mélanie; Arpin, Christophe; Walzer, Thierry; Leverrier, Yann; Marvel, Jacqueline
Immune signatures of protective spleen memory CD8 T cells Article de journal
Dans: Sci Rep, vol. 6, p. 37651, 2016, ISSN: 2045-2322.
@article{pmid27883012,
title = {Immune signatures of protective spleen memory CD8 T cells},
author = {Lilia Brinza and Sophia Djebali and Martine Tomkowiak and Julien Mafille and Céline Loiseau and Pierre-Emmanuel Jouve and Simon de Bernard and Laurent Buffat and Bruno Lina and Michèle Ottmann and Manuel Rosa-Calatrava and Stéphane Schicklin and Nathalie Bonnefoy and Grégoire Lauvau and Morgan Grau and Mélanie Wencker and Christophe Arpin and Thierry Walzer and Yann Leverrier and Jacqueline Marvel},
doi = {10.1038/srep37651},
issn = {2045-2322},
year = {2016},
date = {2016-11-01},
urldate = {2016-11-01},
journal = {Sci Rep},
volume = {6},
pages = {37651},
abstract = {Memory CD8 T lymphocyte populations are remarkably heterogeneous and differ in their ability to protect the host. In order to identify the whole range of qualities uniquely associated with protective memory cells we compared the gene expression signatures of two qualities of memory CD8 T cells sharing the same antigenic-specificity: protective (Influenza-induced, Flu-TM) and non-protective (peptide-induced, TIM) spleen memory CD8 T cells. Although Flu-TM and TIM express classical phenotypic memory markers and are polyfunctional, only Flu-TM protects against a lethal viral challenge. Protective memory CD8 T cells express a unique set of genes involved in migration and survival that correlate with their unique capacity to rapidly migrate within the infected lung parenchyma in response to influenza infection. We also enlighten a new set of poised genes expressed by protective cells that is strongly enriched in cytokines and chemokines such as Ccl1, Ccl9 and Gm-csf. CCL1 and GM-CSF genes are also poised in human memory CD8 T cells. These immune signatures are also induced by two other pathogens (vaccinia virus and Listeria monocytogenes). The immune signatures associated with immune protection were identified on circulating cells, i.e. those that are easily accessible for immuno-monitoring and could help predict vaccines efficacy.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bachy, Emmanuel; Urb, Mirjam; Chandra, Shilpi; Robinot, Rémy; Bricard, Gabriel; Bernard, Simon; Traverse-Glehen, Alexandra; Gazzo, Sophie; Blond, Olivier; Khurana, Archana; Baseggio, Lucile; Heavican, Tayla; Ffrench, Martine; Crispatzu, Giuliano; Mondi`ere, 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 Article de journal
Dans: J. Exp. Med., vol. 213, no. 5, p. 841–857, 2016.
@article{Bachy2016-jl,
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 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 Mondi`ere 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},
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 V$delta$1 TCR-expressing PTCL. These results define a new
subtype of PTCL and pave the way for the development of blocking
anti-CD1d antibody for therapeutic purposes in humans.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
neoplasms with poor prognosis, lack of effective therapies, and a
largely unknown pathophysiology. Identifying the mechanism of
lymphomagenesis and cell-of-origin from which PTCLs arise is
crucial for the development of efficient treatment strategies. In
addition to the well-described thymic lymphomas, we found that
p53-deficient mice also developed mature PTCLs that did not
originate from conventional T cells but from CD1d-restricted NKT
cells. PTCLs showed phenotypic features of activated NKT cells,
such as PD-1 up-regulation and loss of NK1.1 expression.
Injections of heat-killed Streptococcus pneumonia, known to
express glycolipid antigens activating NKT cells, increased the
incidence of these PTCLs, whereas Escherichia coli injection did
not. Gene expression profile analyses indicated a significant
down-regulation of genes in the TCR signaling pathway in PTCL, a
common feature of chronically activated T cells. Targeting TCR
signaling pathway in lymphoma cells, either with cyclosporine A
or anti-CD1d blocking antibody, prolonged mice survival.
Importantly, we identified human CD1d-restricted lymphoma cells
within V$delta$1 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.