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Articles by Antoine Menoret
Autoregulated splicing of TRA2β programs T cell fate in response to antigen-receptor stimulation
Editor’s summary RNA-binding proteins (RBPs) fine-tune gene expression. Some RBPs, such as TRA2β, amplify their own protein abundance by removing, or skipping, ultraconserved poison exon (PE) elements from their gene transcripts. Karginov et al. found that high-affinity ligands for the T cell receptor (TCR) stimulated PE skipping in the TRA2β transcript in CD8 T cells.
Endothelial Immunosuppression in Atherosclerosis : Translational Control by Elavl1/HuR
Abstract Atherosclerotic plaques are defined by the accumulation of lipids and immune cells beneath the endothelium of the arterial intima. CD8 T cells are among the most abundant immune cell types in plaque, and conditions linked to their activation correlate with increased levels of cardiovascular disease. As lethal effectors of the immune response, CD8 T cell activation is suppressed at multiple levels.
CD8+ T cell depletion prevents neuropathology in a mouse model of globoid cell leukodystrophy
Toward the goal of characterizing the CD8+ T cell populations in this disease model, our use of TCR phenotyping, scRNAseq, and profiling of cytokines have generated salient findings. First, TCR profiling of Vβ on CD8+ T cells did not identify an obvious clonal expansion of the populations analyzed. It is important to qualify that the approach used was not exhaustive and we did note that differences within a yet-to-be-defined Vβ subpopulation may yield a unique clonal population.
Astrocytic TIMP-1 regulates production of Anastellin, a novel inhibitor of oligodendrocyte differentiation and FTY720 responses
New Results doi: https://doi.org/10.1101/2023.02.17.529003 Abstract Astrocyte activation is associated with neuropathology and the production of tissue inhibitor of metalloproteinase-1 (TIMP1). TIMP1 is a pleiotropic extracellular protein that functions both as a protease inhibitor and as a growth factor.
Extracellular vesicle fibrinogen induces encephalitogenic CD8+ T cells in a mouse model of multiple sclerosis
Significance In this report, we show that fibrinogen, identified by proteomics to be present in blood plasma extracellular vesicles (EVs), is sufficient and required for autoimmune-mediated spontaneous relapsing disease activity in a murine model of multiple sclerosis (MS). Unique to this model is that plasma EVs induced CD8-mediated disease.
Costimulation Induces CD4 T Cell Antitumor Immunity via an Innate-like Mechanism
Highlights • Costimulatory agonists enhance dendritic cell-mediated CD4 T cell function • Costimulated CD4 T cells respond in an innate-like manner to IL-1 family cytokines • The IL-1 family member IL-36 promotes TCR-independent antitumor CD4+ helper function Summary Chronic exposure to tumor-associated antigens inactivates cognate T cells, restricting the repertoire of tumor-specific effector T cells.
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