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Séminaires de Mai 2012 du Centre de Recherche des Cordeliers

Sauf indications, les séminaires du Centre de Recherche des Cordeliers ont lieu au, 15 rue de l’Ecole de médecine, Paris 75006, dans l’amphithéâtre BILSKI-PASQUIER à 12h
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Vendredi 4 mai 2012 : 12h - Amphithéâtre Bilski-Pasquier
Anne-Marie SCHMITT-VERHULST, CIML, université de Marseille
T cell exhaustion in inflammatory melanoma: can it be reversed ?
A germline mutation or deletion in the gene encoding the tumor suppressors p16INK4A/p14ARF is frequently observed in melanoma-prone families. Human melanoma lesions that arise in the absence of familial genetic predisposition often exhibit both loss of the tumor suppressors and activating mutations in genes in the RAS/BRAF/MAPK pathway. We developed TiRP mice in which conditional “Cre-estrogen receptor/LoxP” technology restricts the Ink4a/Arf deletion and the expression of both H-RasG12V and a natural tumor antigen (TA) to melanocytes. Melanomas developing in these mice express the neural crest marker S100, are deleted at the Ink4a/Arf locus and express transcripts for H-RasG12V as well as the cancer-germline encoded TA P1A. In this model amelanotic melanomas develop rapidly, together with the accumulation of host cells with “immunosuppressive” characteristics, including tumor infiltrating myeloid cells expressing Arginase-1 and Ptgs2/Cox2. In addition, melanoma-produced cytokines appear to induce a STAT3-dependent pro-oncogenic inflammation and inhibition of Th1-type immune responses. The TiRP melanomas are infiltrated by activated T cells lacking effector molecules such as granzyme B. These cells have an ”exhausted“ phenotype, expressing Programmed Death-1 (PD-1), an inhibitory receptor characteristic of chronically stimulated T cells, as well as many other potentially inhibitory receptors (gene array data). In view of the multiplicity of inhibitory surface receptors that appear to be expressed on melanoma-infiltrating T cells in patients, as well as in the induced melanoma in TiRP mice, we sought to design an approach to modify intracellular components in CD8 T cells to dampen the negative signaling effects rather than use extra-cellular blocking reagents to a constellation of surface molecules. To this end, we recently investigated protocols of adoptive T cell therapy which provide increased cytokine receptor signaling by intrinsic means to attempt at overcoming immunosuppression mediated by PD-1-like molecules, as well as that resulting from activation of the STAT3 and TGF-b pathways and from arginine depletion.
Invitée par Catherine FRIDMAN
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Lundi 7 Mai 2012 : 12h - Attention Amphithéâtre Gustave Roussy
SEMINAIRE EXCEPTIONNEL de l’équipe 13 et de l'European Academy of Tumor Immunology et du Labex ImmunoOnco

Mark SMYTH, Peter MacCallum Cancer Centre, Victoria, Australie

Titre non communiqué
Invité par Catherine FRIDMAN et Guido KROEMER
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Vendredi 11 Mai 2012 : 12h - Amphithéâtre Bilski-Pasquier
Pierre PIAZZA, Université de Cergy-Pontoise
Enjeux des nouvelles technologies d'identification
Invité par Danièle LACASA
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Vendredi 25 Mai 2012 : 12h  Amphithéâtre Bilski-Pasquier
Stéphane WALRAND, UMR 1019, INRA, Université de Clermont 1, Clermont-Ferrand
 
Vieillissement musculaire et généralité sur le vieillissement
Invité par Joan CLÉMENT
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