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Quorum sensing is the regulation of gene expression programmes in response to changes in population density. It is probably best recognized as a mechanism through which bacterial communities can synchronize behaviours, such as biofilm formation and bioluminescence. This Comment article highlights the emerging evidence suggesting that quorum sensing also contributes to the regulation of immune cell responses.
The metabolism and maintenance of natural killer (NK) cells is regulated by a previously uncharacterized transcription factor called regulatory factor X7 (RFX7).
Two papers show that combining IL-1 blockade with chimeric antigen receptor T cell therapy for cancer can prevent the induction of a potentially lethal ‘cytokine storm’.
Thirumala-Devi Kanneganti describes a 2002 study by Jürg Tschopp and colleagues that first described the multiprotein, caspase-activating inflammasome complex that drives the maturation and secretion of IL-1β.
The long-term survival of HIV-1-infected CD4+ T cells is shown to be controlled by the anti-apoptotic protein BIRC5 and its upstream regulator OX40, which suggests new therapeutic targets to reduce the size of the viral reservoir.
Gabrielle Belz describes a 2002 paper by Iyer et al. that linked cellular nutrient levels in cytotoxic T cells with their ability to mount a vigorous response.
TLR9-mediated signalling induces type I IFN production through the direct recruitment of IKKα to a signalling platform anchored by the autophagy protein LC3.
The metabolite itaconate induces electrophilic stress that induces an antioxidant response and regulates secondary TLR transcriptional responses and IL-17-driven pathology.