23-11-19, Metz devant l'hôtel de ville : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57013

23-11-19, Metz devant l'hôtel de ville : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57014

23-11-19, Metz, devant l'hôtel de ville : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57015

[23-11-19] Metz, défilé des troupes [sur la place d'Armes] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57016

23-11-19, Metz, vue générale sur la place d'Armes : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57017

[23-11-19] Metz, à l'hôtel de ville : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57018

[23-11-19] Metz, défilé devant la cathédrale sur la place d'Armes : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57019

23-11-19, Pont-à-Mousson, remise de la Croix de guerre [en présence de M. Poincaré] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57020

23-11-19, Pont-à-Mousson, remise de la Croix de guerre [en présence de M. Poincaré] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57021

23-11-19, Pont-à-Mousson, remise de la Croix de guerre : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57022

23-11-19, Pont-à-Mousson, remise de la Croix de guerre : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57023

23-11-19, Pont-à-Mousson, remise de la Croix de guerre : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57024

Lack of Mycobacterium tuberculosis-specific interleukin-17A-producing CD4(+) T cells in active disease.

Protective immunity to Mycobacterium tuberculosis (Mtb) is commonly ascribed to a Th1 profile; however, the involvement of Th17 cells remains to be clarified. Here, we characterized Mtb-specific CD4(+) T cells in blood and bronchoalveolar lavages (BALs) from untreated subjects with either active tuberculosis disease (TB) or latent Mtb infection (LTBI), considered as prototypic models of uncontrolled or controlled infection, respectively. The production of IL-17A, IFN-γ, TNF-α, and IL-2 by Mtb-specific CD4(+) T cells was assessed both directly ex vivo and following in vitro antigen-specific T-cell expansion. Unlike for extracellular bacteria, Mtb-specific CD4(+) T-cell responses lacked immediate ex vivo IL-17A effector function in both LTBI and TB individuals. Furthermore, Mtb-specific Th17 cells were absent in BALs, while extracellular bacteria-specific Th17 cells were identified in gut biopsies of healthy individuals. Interestingly, only Mtb-specific CD4(+) T cells from 50% of LTBI but not from TB subjects acquired the ability to produce IL-17A following Mtb-specific T-cell expansion. Finally, IL-17A acquisition by Mtb-specific CD4(+) T cells correlated with the coexpression of CXCR3 and CCR6, currently associated to Th1 or Th17 profiles, respectively. Our data demonstrate that Mtb-specific Th17 cells are selectively undetectable in peripheral blood and BALs from TB patients.

Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation.

Interleukin-1β (IL-1β) is a potent inflammatory cytokine that is usually cleaved and activated by inflammasome-associated caspase-1. To determine whether IL-1β activation is regulated by inhibitor of apoptosis (IAP) proteins, we treated macrophages with an IAP-antagonist "Smac mimetic" compound or genetically deleted the genes that encode the three IAP family members cIAP1, cIAP2, and XIAP. After Toll-like receptor priming, IAP inhibition triggered cleavage of IL-1β that was mediated not only by the NLRP3-caspase-1 inflammasome, but also by caspase-8 in a caspase-1-independent manner. In the absence of IAPs, rapid and full generation of active IL-1β by the NLRP3-caspase-1 inflammasome, or by caspase-8, required the kinase RIP3 and reactive oxygen species production. These results demonstrate that activation of the cell death-inducing ripoptosome platform and RIP3 can generate bioactive IL-1β and implicate them as additional targets for the treatment of pathological IL-1-driven inflammatory responses.