An ancient integration of an endogenous retroelement in the gene encoding PD-L1 is exapted to generate a soluble form that antagonises the suppressive function of the membrane-bound form.
Metabolic switches between oxidative phosphorylation and aerobic glycolysis plus glutaminolysis direct T cell function by altering the flux of glucose and glutamine to N-glycosylation.
A disease-associated polymorphism in a related protein that regulates neurotransmitter release reveals that antiviral protein IFITM3 forms oligomers to rigidify membranes and inhibit virus fusion with cells.
IFNγ increases the responsiveness of human B cells to IL-2, TLR7/8 and IL-21 signals and therefore enhances antibody production in inflammatory settings associated with autoimmune or chronic disease.
Systemic hypoxia model reveals the detrimental effect of hypoxia on mitochondrial biogenesis in activated T-cells and points at a new approach for improving viral resistance in patients with respiratory diseases.
Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.
The association of atypical memory B-cells and autoimmune antibodies (anti-phosphatidylserine) with hemoglobin levels in malaria patients uncovers a novel mechanism for the human malaria-induced anemia previously identified in mice.
