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Cells closely monitor mitochondrial status. Liu and colleagues show that the kinase Jnk2 regulates mitophagy by inhibiting smARF. Loss of Jnk2 results in defective mitophagy and enhanced ROS generation during hypoxia, which leads to enhanced inflammasome activation.
The mechanisms that control activation of the AIM2 inflammasome by cytosolic bacteria are unclear. Kanneganti and colleagues demonstrate that a pathway involving the transcription factor IRF1 is required for the activation of AIM2.
How host cells induce the release of DNA from cytosolic bacteria is unclear. Broz and colleagues show that the guanylate-binding proteins GBP2 and GBP5 trigger bacteriolysis in infected host cells and thereby allow recognition by the sensor AIM2.
Ezh2 is a protein methylase that epigenetically modifies chromatin. Su and colleagues identify a cytoplasmic role for Ezh2 whereby it controls the extravasation of innate leukocytes through methylation of talin and thereby influences inflammatory responses in vivo.
Visceral adipose tissue (VAT) inflammation drives obesity-induced insulin resistance. Polić and colleagues show that VAT NK cells sense obesity-induced adipose tissue stress and drive inflammation through the production of interferon-γ.
IL-7 is known to control the survival of immature DN thymocytes before β-selection. Guidos and colleagues show that during β-selection, IL-7 controls the growth and differentiation of thymocytes, in part by repressing the transcription factor Bcl-6.
Plants have a vast array of pattern-recognition receptor to detect microbial ligands, but how they sense lipopolysaccharide has remained unknown. Ranf et al. identify the receptor-like kinase SD1-29 as a de facto pattern-recognition receptor for lipopolysaccharide in Arabidopsis.
IL-37 is a member of the IL-1 family with profound anti-inflammatory functions. Nold and colleagues identify the receptor for IL-37 and clarify the molecular nature of the anti-inflammatory pathway induced by this cytokine.
Fan and colleagues show that Sox2, already known to function as a transcription factor that controls lineage specification during embryogenesis, also has a role as a cytosolic and sequence-specific sensor of bacterial DNA in neutrophils.
Tissue-resident memory T cells (TRM cells) provide rapid frontline protection from reinfection. Bergsbaken and Bevan identify a gut TRM cell population generated via an unconventional pathway that is protective against a natural mouse intestinal pathogen.
The RNA-binding protein HuR post-transcriptionally regulates mRNA splicing. Turner and colleagues demonstrate that HuR serves a critical role in thymus-independent antigen responses by regulating the fate of genes related to B cell energy use.
PLVAP is a blood vessel endothelium marker of uncertain function. Salmi and colleagues demonstrate that PLVAP is also expressed on lymphoid endothelial cells, where it regulates the entry of antigen and lymphocytes into the lymph nodes.
PtpA is a secreted mycobacterial protein and virulence factor. Liu and colleagues demonstrate that PtpA suppresses signaling by cells of the innate immune system by coopting the activity of host ubiquitin.
CD1a presents a broad repertoire of lipid-based antigens. Rossjohn and colleagues show that the TCR docks over CD1a in a manner that precludes contact with permissive antigens, while nonpermissive antigens disrupt the TCR-CD1a contact.
The mechanisms of secondary changes in antibody repertoires remain unclear. McHeyzer-Williams and colleagues define the stages of reentry of class-switched memory B cells into germinal centers to remodel existing antibody specificities.
Inflammation needs to be carefully controlled to prevent immunopathology. Zhou and colleagues demonstrate that the kinase MST4 dampens inflammation in a nonredundant way by targeting the activity of the key proinflammatory signaling molecule TRAF6.
iTreg cells and TH17 cells share developmental steps, but their cellular fate depends on environmental cues. Weaver and colleagues show that IL-1 signaling alters the STAT3-STAT5 balance to skew cellular differentiation towards TH17 CD4+ T cells.
The classification of some subsets of innate lymphoid cells (ILCs) is unclear. Colonna and colleagues use transcriptional profiling to show unique gene-expression patterns for some ILCs and overlapping patterns between ILC1 and NK cells.
Long intergenic noncoding RNAs (lincRNAs) contribute to the regulation of gene expression. Pagani and colleagues identify hundreds of unique lincRNAs expressed in human lymphocytes and demonstrate a role for the lincRNA linc-MAF-4 in the differentiation of CD4+ T cells.
The mechanisms that control the suppressive function of Treg cells in specific tissues are unclear. Bopp and colleagues show that Treg cells have high expression of kinase CK2 and this is critical for their ability to suppress type 2 responses in the lungs.