Seminar Friday 11th December at 2pm JL Requin meeting room
21 February 2014
The next CRCL/CLB seminar will take place Friday, the 11th of December, in the JL Requin meeting room (Cheney D, lower floor) at 2pm. We are pleased to welcome Richard TOMASINI (Cancer research centre of Marseille). More information will be available soon.
Congress and conference in oncology - EACR
11 March 2013
You can find on the EACR website various congresses, symposiums or workshops in the field of oncology research. More information: click here
2014 national calls
02 January 2013
Caspase-1 autoproteolysis is differentially required for NLRP1b and NLRP3 inflammasome function
18 November 2014
In the context of the nucleotide-binding domain and leucine rich repeat pyrin containing 1b (NLRP1b) inflammasome activation by anthrax lethal toxin, we reveal a new role for full-length caspase-1. The work of Baptiste Guey in Dr Virginie Petrilli team directly demonstrates that the caspase-1 45-kDa zymogen is able to process pro–IL-1β and to induce pyroptosis, and that apoptosis-associated speck-like protein containing a CARD is dis- pensable for the activity of the NLRP1b inflammasome. This is in contrast to the NLRP3 inflammasome activity, which is inhibited in the absence of caspase-1 autoproteolyis. Our data, which highlight differential requirements for caspase-1 autoproteolysis in NLRP1b and NLRP3 inflammasome function, may have implications for pathogen recognition and response.
TGF-β prevents T follicular helper cell accumulation and B cell autoreactivity
27 August 2014
T follicular helper (Tfh) cells contribute to the establishment of humoral immunity by controlling the delivery of helper signals to activated B cells; however, Tfh development must be restrained, as aberrant accumulation of these cells is associated with positive selection of self-reactive germinal center B cells and autoimmunity in both humans and mice. The JC Marie labn from the Immunology Virology and inflammation dept of the CRCL, showed that TGF-β signaling in T cells prevented Tfh cell accumulation, self-reactive B cell activation, and autoantibody production. They demonstrated that TGF-β signaling is required for the thymic maturation of CD44+CD122+Ly49+CD8+ regulatory T cells (Tregs), which induce Tfh apoptosis and thus regulate this cell population. Moreover, peripheral Tfh cells escaping TGF-β control were resistant to apoptosis, exhibited high levels of the antiapoptotic protein BCL2, and remained refractory to regulation by CD8+ Tregs. The unrestrained accumulation of Tfh cells in the absence of TGF-β was dependent on T cell receptor engagement and required B cells.Together, these data indicate that TGF-β signaling restrains Tfh cell accumulation and B cell–associated autoimmunity and thereby controls self-tolerance. This work has been published in Journal of Clinical Investigation.
PubMed access: click here