TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
Occluding-junctions form a permeability barrier around the hematopoietic niche in Drosophila that controls the production of immune cells in response to infection by shaping the signalling micro-environment produced by the niche.
RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.
The immune Synergistic/Antagonistic Interaction Learner (iSAIL) resource has the capacity to generate insight into combinatorial immunity, help guide hypothesis generation and further experimentation relevant to basic research and drug therapeutics.
A single-nucleotide I232T polymorphic change in FcγRIIB's transmembrane domain bends FcγRIIB's ectodomains toward cell membrane to allosterically hinder FcγRIIB's ligand association, providing novel molecular mechanism for functional loss of FcγRIIB-I232T.