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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.
Pulendran and colleagues use a systems biology analysis to reveal distinct transcriptional signatures of antibody responses to different classes of human vaccines.
The kinase Csk inhibits basal TCR signaling. Weiss and colleagues reveal a requirement for CD28 costimulation upon Csk inhibition for facilitation of actin remodeling and activation of signaling pathways downstream of the phospholipase PLC-γ1.
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.
High-density lipoprotein (HDL) has beneficial effects in coronary artery disease. Latz and colleagues show that HDL's benefits stem at least in part by activating an anti-inflammatory program dependent on the transcription factor ATF3.
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.
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.
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.
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.
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.
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.
Various receptors alert cells to microbial invasion through the detection of conserved molecular patterns and initiate innate immunity. During infection with Legionella pneumophila, macrophages modulate cytokine responses by downregulating protein synthesis according to the pathogenic potential of the intruder.
Inflammasomes are signaling platforms of the innate immune system that activate proinflammatory cytokines after microbial pathogens are sensed or sterile danger is detected. The kinases Syk and Jnk control inflammasome activation by mediating phosphorylation of the inflammasome adaptor ASC.