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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.
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.
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.
Precursor cells entering the thymus have non-T cell potential, yet T cell development is clearly favored. A mechanism dedicated to repressing conflicting myeloid cell fate early during the establishment of T cell identity has now been found.
Mice immunized with influenza virus in the presence of rapamycin, which blocks the formation of germinal centers, make mostly IgM antibodies that protect against infection with multiple subtypes of influenza virus, including avian viruses.
A signaling module consisting of the adaptor ADAP and the Carma1–Bcl-10–MALT1 (CBM)–TAK1 signalosome has been shown to selectively induce cytokine secretion but not cytotoxicity in natural killer cells.
In a phosphorylation-dependent positive feedback loop, the cytidine deaminase AID amplifies the generation of double-strand DNA breaks, which shows it can also function downstream of deamination.
The hypoxia-inducible factor (HIF) pathway controls diverse aspects of the immunological response. Enhanced HIF activity is able to extend and potentiate the effector response of CD8+ T cells against chronic infections and tumor growth.
Signaling via the interleukin 1 (IL-1) family, particularly by IL-1β, has long been linked to the pathogenesis of atherosclerosis. Findings that atherogenic fatty acids induce IL-1α to promote vascular inflammation identify a key role for this less-well-studied cytokine.
Zinc fingers 1 and 4 of Ikaros have unique functions in the selection of Ikaros target genes, lymphocyte development and the suppression of leukemogenesis.
The transcription factor GATA-3 is expressed in quiescent hematopoietic stem cells (HSCs) with long-term repopulating ability. Stress-mediated activation of HSCs promotes localization of GATA-3 to the nucleus in a manner dependent on the mitogen-activated protein kinase p38α and restricts self-renewal.
In the absence of the SCARF1 scavenger system in mice, the load of 'dangerous' molecules can increase, inducing features of lupus in a sex-dependent process. These findings highlight the interplay of death and sex in the generation of autoimmunity.
A unique complex of the interferon receptor IFNAR1 and interferon-β (IFN-β) has been identified that signals independently of IFNAR2 and induces a distinct set of interferon-inducible genes and downstream IFN-β-specific functional responses.
Small phosphorylated prenyl metabolites are potent activators of γδ T cells in human peripheral blood, but the molecular mechanism underlying their antigenic potency has remained a mystery. New data identify BTN3A1 as a novel antigen-presentation molecule for both microbial and host-derived phosphorylated antigens.
CD11b+ dendritic cells (DCs) represent a subset of classical DCs that require signaling via the receptor Notch2 and lymphotoxin-β receptor and act as obligate source of interleukin 23 for protection against Citrobacter rodentium.
Resistance to infection of the skin with Staphylococcus aureus depends on early production of interleukin 1β (IL-1β) and IL-17A by skin-resident cells. However, several members of the IL-20 subfamily of cytokines (IL-19, IL-20 and IL-24) can inhibit the local generation of those two cytokines.
