Signal transduction articles from across Nature Portfolio

Using a generic ligand system, we show that activation via immunoreceptors is dependent on the size, but not the valency or mobility, of their cell surface ligand. This suggests that they trigger using the kinetic segregation mechanism.

The mechanisms by which antigen triggers B-cell activation are incompletely understood. In this Review, Degn and Tolar discuss the different models of B-cell receptor triggering that have been proposed over the years in the light of recent insights.

Pro-inflammatory signaling during embryonic development is poorly understood. Here, the authors identify that the master inflammatory factor p65 drives cycles of cell quiescence and proliferation to power the development of hematopoietic stem cells.

The inhibitor of kB kinase (IKK) is a central regulator of NF-kB signalling. Here the authors identify a motif conserved in substrates of canonical and alternative NF-kB pathways which mediates docking to catalytic IKK dimers: they show that phosphorylation of the conserved tyrosine suppresses the docking interaction.

Cryogenic electron microscopy determines the structure of a fully assembled, MR1-reactive, human Vγ8Vδ3 TCR–CD3δγε₂ζ₂ complex bound by anti-CD3ε antibody Fab fragments.

Findings show a role for the PU.1–IL-9 axis in T_H9 cells in the pathogenesis of RA.

TNIP1, a previously identified risk factor for autoimmunity, regulates mitochondrial autophagosomal trafficking. Missense mutations in TNIP1 disrupt this regulatory function, yielding a B cell-intrinsic predisposition for TLR7-mediated autoimmunity characterized by IgG4 autoantibodies and the expansion of age-associated B cells.

We show that multivalent epitope display on the surface of viral-sized particles functions as a ‘stand-alone’ danger signal by evading inhibitory pathways to trigger a unique mode of B cell receptor signaling. The activation, survival and proliferation of B cells stimulated with particulate antigen is highly enhanced compared with those stimulated with soluble antigen, and does not require co-stimulation from T cells.

At high doses, the dietary sweetener sucralose interferes with T cell receptor signalling, impairing antitumour and antibacterial T cell responses in mice.