Immunology
Reciprocal regulation of STING and TCR signaling by mTORC1 for T-cell activation and functionCostimulation of T cells through both TCR and STING induces growth inhibition by partially blocking the mTORC1 signals, and leads to IFN-I production through sustained activation of IRF3 and mTORC1 activation.
Viperin controls chikungunya virus–specific pathogenic T cell IFNγ Th1 stimulation in miceThis study shows that Viperin controls the microenvironment pro-inflammatory response and CD4 T cell–mediated pathogenesis during anti-chikungunya virus immune response in mice.
Absence of MHC-II expression by lymph node stromal cells results in autoimmunityMHCII-restricted antigen presentation by lymph node stromal cells is essential for regulatory T-cell proliferation and functions, and for the regulation of autoimmunity.
Dimerization and auto-processing induce caspase-11 protease activation within the non-canonical inflammasomeThis study provides a detailed molecular mechanism for caspase-11 activation within the non-canonical inflammasome, giving new insight into host defence against cytosolic bacterial infection.
Extracellular vesicles from mature dendritic cells (DC) differentiate monocytes into immature DCMature dendritic cells (DC) secrete substantial amounts of vesicles that are primarily ingested by monocytes, leading to differentiation processes in these target cells towards monocyte-derived DC.
Dynamic reorganisation of intermediate filaments coordinates early B-cell activationThis study examines the role of vimentin, a type III intermediate filament, in B-cell function using a combination of in vitro and in vivo assays, including super-resolution microscopic techniques.
Immunoediting is not a primary transformation event in a murine model of MLL-ENL AMLUsing a conditional model of MLL-ENL–driven AML, Dudenhöffer-Pfeifer and Bryder show that NK cell and adaptive immunity influences little on leukemia initiation from normal cells. The data argue against immune escape as a universal primary transformation event in AML.
The expansion in lymphoid organs of IL-4+ BATF+ T follicular helper cells is linked to IgG4 class switching in vivoT follicular helper cells that secrete IL-4 accumulate in lymphoid organs in IgG4-related disease and are linked to IgG4 class switching.