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September 2017

  Message d'Henri Gruffat



Bonne année 2019 à toutes et tous. Je vous souhaite joie, bonheur, santé, mais aussi de belles réussites professionnelles et personnelles. Que tous vos projets se réalisent et soient couronnés de succès individuels et collectifs.
J’espère que nous partagerons ensemble la joie des découvertes au cours des nombreux séminaires que nous organisons. Bonne et heureuse année.


Salle de conférence de l'IBCP

Séminaire externe


“ Interbacterial antagonism: an ancient process that remains full of surprises ”


Joseph MOUGOUS (University of Washington School of Medicine, Seattle, USA)   -- Invited by S. Bigot


Though they are by definition single-celled organisms, bacteria can exhibit properties more often ascribed to multicellular life. Our group aims to identify, characterize, and eventually, exploit, pathways that bacteria use for intercellular communication and competition. In this presentation, I will discuss our recent progress toward understanding the diversity of mechanisms by which antibacterial toxins delivered by assorted specialized secretion systems act upon recipient cells.


Salle des thèses CRC

Séminaire externe

« Microglia at the crossroads of cortical wiring and environmental signals »


Sonia GAREL IBENS, Paris

Host: Pierre Godement


Amphi Pasteur

Séminaire externe

“ B cell antigen receptor signaling in maintenance of mature as well as CLL-like B cells ”


Dr. Elias HOBEIKA - Institute of Immunology – Ulm University Hospital Ulm – RFA
contact :



Expression of a functional B cell antigen receptor (BCR) is essential for the maintenance and differentiation of B cells. It is thus not surprising that multiple B cell-derived malignancies critically depend on BCR-signaling in terms of their development and retention. Accordingly, in chronic lymphocytic leukemia (CLL), inhibition of signaling molecules downstream of the BCR, like the Bruton’s Tyrosine Kinase (BTK) by Ibrutinib, leads to the efficient eradication of the malignant cells. In the presented work, we investigate the importance of the BCR signaling for the maintenance of leukemic B cells derived from the EmTcl-1 mouse model for a CLL-like disease. We report that inactivation of either Igα or Igβ on the EmTcl-1-transgenic background results in a rapid demise of the CLL-like B cells thus demonstrating that BCR-expression and subsequently BCR-signaling are indispensable for the maintenance of CLL-like B cells in vivo. We are now investigating the signaling pathways, which may contribute to the rescue of the BCR-deficient CLL-like B cells from elimination.


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