Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.

Excessive inflammation of the brain in early life predisposes individuals to neurodevelopmental disorders by preventing synapses from developing correctly.

The deubiquitinating enzyme YOD1 binds to the E3 ligase TRAF6 to counteract p62/sequestosome1 mediated pro-inflammatory NF-κB signaling in response to interleukin-1.

Cellular immunological and biochemical analyses reveal how decoy IL-1RII is induced by human CD4⁺ T cells upon TCR-stimulation and regulates the Th17-Treg balance by modulating IL-1β responsiveness in IL-1RI⁺ cells.

Wounded epidermal keratinocytes emit a signal that activates a specialized T-cell in the skin, leading to an increase in hair follicle stem cell numbers that contributes to tissue repair.

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.

Targeting the differentiation regulators and/or AMPs of keratinocytes, rather than targeting immune cells, may be an alternative approach for topical anti-psoriatic treatment, an area with high need for new drugs.

Understudied atypical MAPK, ERK3 controls epithelial secretome and chemotaxis.

c-Maf is a novel key regulator of the type 3-to-1 conversion of CCR6^– ILC3s that controls the functional plasticity of ILC3s by acting as a cell-intrinsic gatekeeper of T-bet expression.

HOIL-1 deficiency in mice results in a severe immunodeficiency that is effectively complemented by chronic infection with a murine gamma-herpesvirus.