@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}

}

@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}

}

@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}

}