Lionel Apetoh
  • E-mail :[email]
  • Phone : + 33 3 80 39 33 71
  • Location : Dijon, France
Last update 2017-08-08 10:31:19.563

Lionel Apetoh PhD Immunology

Course and current status

CURRENT SITUATION

  • 2017 -   Team leader, INSERM UMR1231, Dijon, France.

Research focus: “Regulation of T cell differentiation by nucleic acids 

  • 2012 -   Chargé de recherche de 1ère classe (Research assistant professor in immunology), INSERM UMR1231, Dijon, France. 

POSITIONS

  • 2011-2016  Group leader in Pr. Ghiringhelli’s laboratory, INSERM UMR866, Dijon, France.

Research focus: “CD4 T cell differentiation and cancer”

  • 2008-2010 Postdoctoral research fellow at the Brigham and Womens’ Hospital, Harvard Medical School, Boston, MA, United States

Research project: “Transcriptional regulation of CD4 type 1 regulatory T cells”

Supervisor: Pr Vijay Kuchroo 

  • 2004-2008  PhD in immunology (summa cum laude) defended June 3rd 2008 in Villejuif, France. 

Research project: “Immunogenicity of tumor cell death triggered by anticancer therapies”

PhD Supervisor: Pr Laurence Zitvogel

MAJOR AWARDS

2015 ERC Starting Grant

2015 “Albert Sézary Prize” (French National Academy of Medicine)

2015 “Olga Sain Prize” (Ligue contre le Cancer)


Scientific summary

Our group currently investigates the relationships between CD4 T lymphocytes and anticancer immune responses.

Effector CD4 T cells were initially classified in 1986 by Mossman and Coffman into Th1 and Th2 cells.  Th1 cells limit infections caused by intracellular bacteria while parasitic infections favor Th2 cell expansion. In the setting of cancer immunity, Th1 cell polarization is associated with an effective anticancer immune response in contrast to Th2 cell immunity, which possibly contributes to tumor growth. Novel subsets of CD4 T lymphocytes have now been identified like Th17 cells (secreting IL-17) and Th9 cells (secreting IL-9). These cells are known to be highly proinflammatory in vivo. However, their putative contribution to tumor progression remains incompletely defined. Our group aims to determine the molecular mechanisms that can endow Th17 and Th9 cells with anticancer properties to contemplate the use of these cells in anticancer adoptive T cell therapy.

Team involved in this project :

  • Apetoh Lionel (Research assistant professor in immunology)
  • Baeza Garcia Alvaro (Post-doc)
  • Fournier Carole (Post-doc)
  • Benoit-Lizon Isis (PhD student)
  • Dalzuffo Ludivine (Research assistant)
  • Martin Tiffany (Research assistant)
  • Mélis Andréa (Research assistant)
  • Roussey Aurélie (Research assistant)

 

Selected publications (out of 95):

  • Rivera Vargas T, Cai Z, Shen Y, Dosset M, Benoit-Lizon I, Martin T, Roussey A, Flavell RA, Ghiringhelli F, Apetoh L

Selective   degradation    of   the   PU.1   transcription    factor   during   autophagy   represses differentiation and antitumor activity of Th9 cells. Nat. Commun., 2017, in press.

  • Vegran F, Berger H, Boidot R, Mignot G, Bruchard M, Dosset M, Chalmin F, Rébé C, Dérangère V, Ryffel B, Kato M, Prévost-Blondel A, Ghiringhelli F, Apetoh L 

IRF1 dictates the IL-21-dependent anticancer functions of Th9 cells. Nat. Immunol., 2014 Aug;15(8):758-66.

  • Berger H, Végran F, Chikh M, Gilardi F, Ladoire S, Bugaut H, Mignot G, Chalmin F, Bruchard M, Derangère V, Chevriaux A, Rébé C, Pot C, Ryffel B, Hichami A, Desvergnes B, Ghiringhelli F, Apetoh L

SOCS3 transactivation by PPARg prevents IL-17-driven cancer growth. Cancer Res. , 2013 Jun 15;73(12):3578-90.

  • Bruchard M, Mignot G, Derangère V, Chalmin F, Chevriaux A, Végran F, Boireau W, Simon B, Ryffel B, Connat JL, Kanellopoulos J, Martin F, Rébé C, Apetoh L*, Ghiringhelli F*

Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the NLRP3 inflammasome and promotes tumor growth. Nat. Med., 2013 Jan;19(1):57-64.* Contributed equally

  • Sakuishi K*, Apetoh L*, Sullivan JM, Blazar BR, Kuchroo VK, Anderson AC 

Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity. J. Exp. Med. 2010 Sep 27;207(10):2187-94. *Contributed equally 

  • Apetoh L, Quintana FJ, Pot C, Joller N, Xiao S, Kumar D, Burns EJ, Sherr DH, Weiner HL, Kuchroo VK 

The aryl hydrocarbon receptor interacts with c-Maf to promote the differentiation of type 1 regulatory T cells induced by IL-27. Nat. Immunol. 2010 Sep;11(9):854-61.

  • Apetoh L, Ghiringhelli F, Tesniere A, Obeid M, Ortiz C, Criollo A, Mignot G, Maiuri MC, Ullrich E, Saulnier P, Yang H, Amigorena S, Ryffel B, Barrat FJ, Saftig P, Levi F, Lidereau R, Nogues C, Mira JP, Chompret A, Joulin V, Clavel-Chapelon F, Bourhis J, André F, Delaloge S, Tursz T, Kroemer G and Zitvogel L

Toll-like Receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy. Nat. Med. 2007 Sep:13(9):1050-1059.

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