Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

Engineering cytokines to exhibit different receptor binding dwell times is a useful strategy to decouple their functional pleiotropy and reduce their toxicity in the clinic.

A novel binning approach provides evidence for super-functional T cells with high activation potential and which exhibit Tfh-like functionalities and can help B cells.

A murine adoptive transfer model shows that binary IL-2 and graded CD25 expression tailor the T helper cell response to the antigen amount in vivo.

Expression of two highly regulated subfamilies of the complex multigene family encoding IL-17 cytokines in the purple sea urchin are sequentially activated in a larval gut-associated inflammation model and modulate downstream gene expression in the gut epithelium.

Similar to T cell exhaustion, natural killer cell dysfunction in chronic hepatitis B patients results from deregulated calcium pathway.

Uncovering a mechanism for how inflammatory signaling is opposed by a phosphatase identifies a potential druggable target to treat E. coli sepsis.

Determining that microbiota-deficient mice have increased visceral pain, which can be reversed by restoring microbiota, may lead to novel microbial-based strategies for disorders associated with visceral pain.

The induction of ISG15 during bacterial infection can be independent of Type I Interferons and leads to an increase in the secretion of cytokines known to be critical for bacterial clearance.

Peptide immunotherapy in mice depends upon sustained expression of co-inhibitory protein PD-1 in T cells.