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The sensing of viable pathogens by the receptor TLR8 on human monocytes provides key signals that initiate the differentiation of naive CD4+ T cells into follicular helper T cells. Targeting TLR8 might represent a novel approach for improving immunity following vaccination.
Tumor cells downregulate type I interferon responses through their delivery of immunomodulatory exosomes, which has implications for antiviral suppression in people with cancer.
Large-scale genetic and immunological profiling reveals key environmental and genetic drivers of immunological diversity within the healthy human population.
The transcription factor Hoxb5 is expressed specifically in hematopoietic stem cells, yet its ectopic expression in mouse B cell progenitors induces their conversion into functional T cells in vivo.
ERAdP, an endoplasmic reticulum (ER)-resident protein with similar mechanistic features as the innate immune adaptor STING, controls inflammatory cytokine release, but not that of type I interferon, in response to bacterial cyclic di-AMP.
The transcription factor Aire restrains the transcriptional duration and amplitude of tissue-specific self-antigens by opposing the activity of the chromatin remodeler Brg1—a process required for immune tolerance.
CD8+ tissue-resident memory T cells (TRM cells) in two mucosal tissues, the skin and the female reproductive tract, proliferate in situ to generate a secondary pool of TRM cells that does not exit into the circulation.
Detrimental levels of intracellular reactive oxygen species engage a caspase-independent and non-inflammatory cell death called ‘oxeiptosis’ that serves as an important mechanism in diminishing inflammation.