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

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.

The thioredoxin-1 (Trx1) system promotes inflammation by positively regulating both NLRP3 inflammasome responses, by detoxifying excessive ROS independently of Txnip and NF-κB binding to target DNA.

Inflammation reprograms the citrate cycle in adrenocortical cells leading to altered steroidogenesis.

Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na⁺) channels.

A pattern recognition receptor called toll-like receptor 13 detects pathogens in a manner that is different to that seen in other pathogen sensors.

The vaginal immunoproteome in pregnancy is more predictive of spontaneous preterm birth (sPTB) than maternal characteristics alone, with sPTB cases showing heightened pro-inflammatory profiles accompanied by reduced levels of antimicrobial proteins/peptides.

Expression of an interleukin that is immune suppressive (IL-37) in mice is able to limit inflammation in the brain after acute inflammatory events and prevent loss of cognitive abilities in a mouse model of AD.

Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

Mutated NLRP3 forms cryo-sensitive aggregates that induce inflammasome assembly distinct from the canonical NLRP3 inflammasome.