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The sensing of nucleic acids is pivotal for detecting viral infections. Reinecker and colleagues (p 63) show that the microtubule-associated protein GEF-H1 is activated after the intracellular detection of nucleic acids and is required for antiviral defense against RNA viruses. The original image, generated by Hans-Christian Reinecker and Hao-Sen Chiang, shows GEF-H1 (green) and the microtubule network (red); yellow indicates colocalization of GEF-H1 and a-tubulin.Artwork by Lewis Long.
Studies have linked polymorphisms near the gene encoding interferon-λ3 (IFNL3) to clearance of hepatitis C virus (HCV). One such favorable polymorphism operates by stabilizing IFNL3 mRNA via a decrease in AU-rich element–mediated decay as well as the binding of HCV-induced host microRNAs.
Control of infection with Staphylococcus aureus relies on the production of neutrophil-recruiting chemokines by perivascular macrophages. S. aureus counterattacks by secreting α-hemolysin, which lyses tissue macrophages.
Innate-like T cells are dependent on triggering via the T cell antigen receptor (TCR) for development but subsequently actively alter their TCR responsiveness to allow an innate mode of activation that no longer requires TCR signaling.
The identity of the thymus-seeding progenitor cells has been a matter of debate. Cumano and colleagues report that early and late embryonic progenitor cells differ in their T cell–B cell lineage potential and capacity for population expansion and differentiation.
Paired immunoglobulin-like receptors (PIRs) recognize β2-microglobulin. Munitz and colleagues show that PIR-A and PIR-B have opposing roles in eosinophil development in response to interleukin 5 in the bone marrow.
Weninger and colleagues show that perivascular macrophages are critical for neutrophil migration into skin infected with Staphylococcus aureus and that the pathogen uses hemolysin-dependent killing of these cells as an immune evasion strategy.
Plasmacytoid dendritic cells produce copious amounts of type I interferon in response to viral infection. Brown and colleagues show that the homeostasis and function of these cells are regulated by the microRNA miR-126.
RIG-I–like receptors are important inducers of innate immunity. Reinecker and colleagues find that activation of the microtubule-associated guanine nucleotide exchange factor GEF-H1 is essential for sensing of foreign RNA by these receptors.
Polymorphisms near genes encoding members of the IFN-λ family are associated with susceptibility or resistance to hepatitis C virus. Savan and colleagues show that differences in the stability of transcripts of those genes underlie the mechanism of resistance to that virus.
T cell hyporesponsiveness is generally framed in terms of tolerance induction. Hayday and colleagues show that attenuating TCR responsiveness is also critical for the development of innate-like T cells that mediate the surveillance of dysregulated tissues.
Lymphocyte function is regulated by phosphatidylinositol-dependent pathways. Uzel and colleagues identify a cohort of immunodeficient patients with hyperactive phosphatidylinositol-3-OH kinase activity due to mutant p110δ subunits, which results in enhanced senescence of cells of the immune system.
Dendritic cells (DCs) that orchestrate mucosal immunity have been studied in mice. Lahl and colleagues characterize human gut DC populations and define their relationship to previously described human and mouse DCs.