Homeostatic innate lymphoid cell abundance, adjusted for age and sex, correlates inversely with COVID-19 severity in adults and children.

The E3 ubiquitin ligase complex linear ubiquitin chain assembly complex (LUBAC) forms a branched chain on linear ubiquitin chains depending on the RING-in-between-RING-type E3 ligase heme-oxidized IRP2 ubiquitin ligase 1 (HOIL-1L).

The function of the SARS-CoV-2 spike is controlled by allosterically modulating the dynamics of the receptor-binding domain.

The adaptor proteins FADD and TRADD play an important role in the Sharpin-dependent anti-apoptosis signaling pathway in keratinocytes and regulate skin homeostasis.

ADP-ribosylation factor-like GTPase 15, an atypical small GTPase, binds to cystathionine-β-synthase-pair domain divalent metal cation transport mediator (CNNM) membrane proteins to inhibit divalent cation efflux by CNNM proteins and influx by transient receptor potential ion channel subfamily M member 7.

Skin inflammation in Sharpin-deficient mice is primarily due to TNFR1-dependent apoptosis, but necroptosis appears to play a bigger role in inflammation of internal organs.

A cell-free system combined with cell-based assays elucidate the biochemical mechanism of signal transduction mediated by the mitochondrial protein MAVS and delineates the role of ubiquitin E3 ligases in antiviral innate immune responses.

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

Combined tissue clearing, 3D-immunofluorescence, and electron tomography spatially revealed the dynamics of early HIV-1 spread within lymphoid tissues of humanized mice at the resolution of single cells and individual virions.