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How T cell cytotoxic activity is induced remains incompletely defined. Yasutomo and colleagues now show that Notch2 signals, in direct cooperation with the transcription factor CREB1, promote granzyme B expression.
The molecular components of inflammasomes and what they sense are poorly defined. Vance and colleagues now show the carboxy-terminal 35 amino acids of flagellin activate the inflammasome in a Naip5-dependent way.
Microbial sensors activate the Toll pathway in flies. Reichhart and colleagues identify the serine protease Grass, which acts in parallel with Persephone to cleave Toll-activating Spatzle in response to Gram-positive bacteria and fungi.
Uncontrolled TLR signaling results in excessive inflammation. Arthur and colleagues show that the kinases MSK1 and MSK2 orchestrate a feedback loop involving interleukin 10 and the phosphatase DUSP1 to control TLR4 signaling.
The function of the kinase p38α in inflammation is unclear. Park and colleagues show that p38α exerts pro- or anti-inflammatory effects depending on the cell type in which it is expressed and the stimulus eliciting its activation.
The mechanisms controlling expression of the stress-induced NKG2D ligands MICA and MICB are not fully understood. Mandelboim and colleagues suggest that microRNAs maintain low MICA and MICB expression in the absence of cell stress.
Lungs are continually challenged by exposure to airborne particles and microbes, yet they resist overt inflammatory responses. Hussell and colleagues show that this 'quiescent' state requires CD200-CD200R interactions between alveolar macrophages and lung tissues.
Invariant natural killer cells recognize glycolipids presented by CD1d molecules and can mediate rapid innate responses. Sant'Angelo and colleagues show that these cells express the transcription factor PLZF, which is required for their innate effector function.
The function of the adaptor protein TRADD is uncertain. Teams led by Pasparakis and Liu solidify TRADD's function in TNF receptor signaling and extend its influence to TRIF-dependent Toll-like receptor pathways.
The function of the adaptor protein TRADD is uncertain. Teams led by Pasparakis and Liu solidify TRADD's function in TNF receptor signaling and extend its influence to TRIF-dependent Toll-like receptor pathways.
The events leading to the inflammation and tissue damage associated with Alzheimer's disease are unclear. Golenbock and colleagues now show that amyloid-β activates the NALP3 inflammasome, which triggers the release of proinflammatory and neurotoxic factors.
Activation of the NALP3 inflammasome induces interleukin 1β production and inflammation. Latz and colleagues show that silica uptake followed by lysosome disruption and cathepsin B release activates the NALP3 inflammasome.
Inhibitory receptors antagonize natural killer cell cytotoxicity. Ge and colleagues show that the scaffold protein β-arrestin 2 recruits the phosphatases SHP-1 and SHP-2 to the inhibitory receptor KIR2DL1 to enhance 'downstream' inhibitory signaling.
The TNF receptor 4-1BB functions as a costimulatory molecule in T cells. Croft and colleagues show that binding of 4-1BB to its ligand regulates the production of dendritic cells by inhibiting myelopoiesis.
The importance of autophagy in host survival during intracellular bacteria infection remains unclear. Kurata and colleagues show that in drosophila, autophagy initiated by the pattern-recognition receptor PGRP-LE promotes survival after Listeria monocytogenes infection.
The enzyme superoxide dismutase 1 (SOD1) protects cells from superoxide toxicity. Zychlinsky and colleagues find that post-translational glutathionylation of caspase-1 by SOD1 triggers caspase-1 activation and subsequent interleukin 1β production.
Essential for antigen-driven T cell responses, the cortactin homolog HS1 may also influence natural killer cell biology. Butler and colleagues identify functions for cortactin in natural killer cell cytotoxicity, adhesion and chemotaxis.
To kill pathogens, neutrophils must be able to transmigrate into tissues. Xu and colleagues show that the kinase MYLK, by phosphorylating Pyk2, is required for neutrophils to reach sites of infection.
The Toxoplasma gondii peptides recognized by protective CD8+ T cells remain uncharacterized. Shastri and colleagues identify an immunodominant T. gondii peptide generated by a mechanism dependent on the endoplasmic reticulum aminopeptidase ERAAP.
The transcription factor Ikaros has many functions essential for hematopoiesis. Singh and colleagues show that Ikaros is required for RAG recombinase expression and regulation of VH accessibility in developing B cells.