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ASC has emerged as an adaptor for inflammasome sensors in cells of the innate immune response. New inflammasome-independent roles have been identified for ASC in the control of adaptive immunity; these include the post-transcriptional regulation of cytoskeletal rearrangements.
The sensing of pathogen-associated DNA in the cytoplasm is an important trigger of host-defense responses that include the production of type I interferon. A new study suggests that the DExDc helicase DDX41 may function in dendritic cells as a DNA sensor to activate STING-dependent innate immune responses.
In addition to its recognized function as an enzyme that catalyzes tryptophan, indoleamine 2,3-dioxygenase (IDO) acts as an intracellular signal transducer, in response to transforming growth factor-β (TGF-β), to induce a stably regulatory phenotype in plasmacytoid dendritic cells.
Tuberins, the tumor-suppressor proteins that regulate signaling via the kinase mTOR, now emerge as essential enforcers of T cell quiescence that promote survival.
Proinflammatory signaling by the interleukin 17 receptor requires the adaptor Act1. Two studies identify an additional function for Act1 and identify new participants that regulate the inflammatory effects of IL-17.
The kinase IKKα has a well-described activating role in the noncanonical transcription factor NF-κB pathway. Evidence now suggests that IKKα also inhibits the canonical NF-κB pathway by phosphorylating the scaffold protein TAX1BP1 to promote the assembly of the A20 ubiquitin-editing complex.
Innate immune responses need to be tightly controlled to avoid autoimmune and inflammatory diseases. The atypical orphan nuclear receptor SHP has now been identified as a negative regulator of Toll-like receptor–induced activation of the transcription factor NF-κB.
The generation of Ly6C− patrolling monocytes requires the transcription factor NR4A1 (Nur77). This finding provides insight into the development and function of these blood-resident cells.
Systems biology has emerged as a promising research strategy that can be applied to vaccine development. This approach can lead to the identification of new mechanisms and predictors of inactivated vaccine immunogenicity.
New data show that the interferon-induced gene product IFIT1 is a sensor for 5′-triphosphorylated RNA of viral origin and that it functions within a larger IFIT complex to inhibit viral replication.
The T cell antigen receptor is functionally coupled to many kinases and adaptor proteins. Analysis of the spatiotemporal organization of the T cell antigen receptor signaling cascade suggests that adaptor-containing intracellular vesicles are essential for proper signal propagation.
Although the role of adaptive immunity in asthma is well characterized, there is relatively little understanding of the contribution of innate immunity to asthma. Studies now suggest that interleukin 13 produced by innate natural helper cells in the lungs has a substantial and underappreciated role in asthma exacerbation.
In response to inhaled pathogens, lymphoid tissues can form in the lung. The driving force behind this organogenic process turns out to be interleukin 17–mediated activation of lung stromal cells.
This report describes advances in the understanding of how microbes elicit and evade immune responses and the sensing of pathogens by host cells that leads to the activation and production of intra- and extracellular signaling molecules.
