@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}

}

@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}

}

@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}

}