9 research outputs found
Mise au point d'une composition de béton de référence pour recherches et essais en laboratoire
Progress report on the work of the permanent committee on concrete and enquiry among RILEM members
The determination of the permeability of concrete to oxygen by the Cembureau method—a recommendation
Measurement of the fracture energy using three-point bend tests: Part 3—influence of cutting theP-δ tail
NF-κB subunits RelA and c-Rel selectively control CD4⁺ T cell function in multiple sclerosis and cancer
The outcome of cancer and autoimmunity is often dictated by the effector functions of CD4+ conventional T cells (Tconv). Although activation of the NF-κB signaling pathway has long been implicated in Tconv biology, the cell-autonomous roles of the separate NF-κB transcription-factor subunits are unknown. Here, we dissected the contributions of the canonical NF-κB subunits RelA and c-Rel to Tconv function. RelA, rather than c-Rel, regulated Tconv activation and cytokine production at steady-state and was required for polarization toward the TH17 lineage in vitro. Accordingly, RelA-deficient mice were fully protected against neuroinflammation in a model of multiple sclerosis due to defective transition to a pathogenic TH17 gene-expression program. Conversely, Tconv-restricted ablation of c-Rel impaired their function in the microenvironment of transplanted tumors, resulting in enhanced cancer burden. Moreover, Tconv required c-Rel for the response to PD-1-blockade therapy. Our data reveal distinct roles for canonical NF-κB subunits in different disease contexts, paving the way for subunit-targeted immunotherapies