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Pre-existing enhancers interpret T cell signaling strength in an analogue manner to direct quantitative changes in gene expression within the context of an overall digital response.

AXL enables the priming of the antiviral adaptive immune response by limiting the production of type I interferons in dendritic cells.

Notch1 activates autophagy to regulate the survival of T-regulatory cells from mice.

By joining the Skp1-Cul1-Rbx1 SCF complex, Fbxo21 interacts with ASK1 and mediates Lys29-linkage of ASK1, leading to type I IFN production.

Asymmetrical expression dictates functional dominance of one STAT5 paralog at cellular and tissue levels despite redundancy at molecular and genomic levels.

A signal for inflammatory cell death is induced by the disruption of cellular metabolism.

An experimental approach allowing characterization of viral RNA ligands recognized by RIG-I-like receptors during infection by any RNA viruses is established and validated.

The scanning-assisted clustering mechanism of IFI16 not only allows efficient assembly on exposed foreign-dsDNA, but also suppresses the engagement of chromatinized self-dsDNA.

Insects use serotonin signaling in blood cells to help defend themselves against pathogens.

Controlled neo-glycosylation of antigens can influence intracellular routing of antigens and the nature and strength of immune response, and should therefore be considered as a major determinant in the design of vaccines against cancer and infectious diseases.