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Ligation of the Toll-like receptor TLR7 in human CD4+ T cells elicits an anergic state that may contribute to CD4+ T cell hyporesponsiveness after infection with human immunodeficiency virus type 1 and may also enhance propagation of this virus.
Virus-triggered type I interferon induces the lysine methyltransferase Setdb2; this then generates repressive histone marks on the promoters of genes encoding molecules important for antibacterial immunity. This process can contribute to influenza virus–associated bacterial superinfection.
T cells with increased self-reactivity and marked by high expression of the negative regulator CD5 differ in gene-expression patterns and are poised for greater bursts of proliferation when they encounter foreign antigens.
Vesicular stomatitis virus, a single-stranded RNA virus, triggers activation of the serine-threonine kinases RIP1 and RIP3, which damages mitochondria by activating the GTPase DRP1. This results in excessive production of reactive oxygen species and subsequent activation of the NLRP3 inflammasome.
Chitinase-like proteins are associated with type 2 immune responses and the 'wound-healing' pathway, but their role has remained unclear. Studies have now highlighted their contribution to IL-17 production and their link to neutrophil activity required for the control of helminth infection.
The combination of machine-learning tools and mass-cytometry measurements of more than 30 protein markers per cell comprehensively maps cell identity in the heterogeneous myeloid cell system and reveals the global effect of deletion of the gene encoding the receptor for the growth factor GM-CSF.
Humans deficient in the adaptor MyD88 or the kinase IRAK4 suffer from primary immunodeficiency. Blood cells from these patients show defective induction of specific subsets of genes after exposure to microbial stimuli in vitro.
Clusters of dermal dendritic cells and T cells are required for efficient activation of T cells in skin following hapten sensitization via a process dependent on interleukin 1α (IL-1α) and the chemokine CXCL2 produced by macrophages.
Acute ablation of T cell antigen receptors (TCRs) in regulatory T cells (Treg cells) impairs the suppressive activity of these cells, even though they retain expression of Foxp3 and CD25. TCR signaling imparts a critical role in the suppressive function of Treg cells.
Alveolar macrophages derive from fetal monocytes that seed the lungs during late embryogenesis. The cytokine GM-CSF expressed in the developing lungs induces expression of the nuclear receptor PPAR-γ, which in turn 'instructs' the differentiation of alveolar macrophage.
Neutrophil function is perhaps best studied in bacterial infection, during which they are directly involved in pathogen killing. After helminth invasion, however, neutrophils acquire an alternative transcriptional profile that allows them to 'train' macrophages to acquire long-term protective features.
ThPOK, the critical transcription factor for differentiation of the helper T cell lineage in the thymus, continues to function as a gatekeeper to maintain helper T cell identity by repressing the transcription factor Runx3 in mature T cells.
Transcriptional profiling of endothelial cells from diverse secondary lymphoid organs reveals distinctions that underlie their functional specification.
A ligand and G protein–coupled receptor activate antimicrobial gene expression in the Caenorhabditis elegans epidermis, in response to wounding and to infection with a fungal pathogen.
AP4, a transcription factor induced by the functionally related transcription factor c-Myc, maintains the cellular metabolic program for the sustained activation and population expansion of CD8+ T cells after the dynamic loss of c-Myc expression.
The unfolded protein response produces modified endogenous RNA substrates for host cytosolic sensors of RNA, which may lead to production of the interferons IFN-α and IFN-β. The accrual of modified RNA is prevented by an RNA nuclease.
Infection with an RNA virus induces the interferons IFN-β and IFN-λ via the adaptor MAVS located in mitochondria, while peroxisomal MAVS selectively activates an IFN-λ response.
Inflammasome-driven inflammation extends into the extracellular space and to neighboring cells through the passive release of specks consisting of the adaptor ASC; this perpetuates the innate immune response and adds a dimension beyond interleukin 1 to autoinflammation.
