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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.
Researchers gathered in Paris at the first European Molecular Biology Organization conference devoted to innate lymphoid cells and discussed recent advances to further understanding of the development, regulation and function of these intriguing cells.
Much of the research on lung immunology has concentrated on classic hematopoietically derived cells of the immune system. In this Focus Review, Alenghat and Whitsett discuss the key innate immunological functions of the respiratory epithelium.
Asthma is typically thought to be a consequence of overreactive type II responses. In this Focus Review, Lambrecht and Hammad discuss the latest thinking on the etiology of asthma and the importance of alternative mechanisms such as ILC2, TH9 and TH17 cells.
Mycobacterial tuberculosis remains a disease of major importance. In this Focus Review, Orme, Robinson and Cooper discuss lung immune responses to mycobacteria and describe how the bacterium can manipulate host immunity to its own ends.
The lungs hosts their own unique populations of macrophages and dendritic cells. In this Focus Review, Kopf, Schneider and Nobs discuss the development and maintenance of these populations in the lungs.
The lungs are the main site of entry for most viral pathogens. In this Focus Review, Chiu and Openshaw discuss adaptive immune responses to lung-tropic viruses and implications for vaccine development.
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.
Mesenchymal stem cells are being considered as potential therapy for the regeneration of damaged tissues. Shi and colleagues review how these cells are influenced by inflammation and their interactions with cells of the immune system.
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.
