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Helicases are vital to the induction of antiviral responses. Cao and colleagues demonstrate that the helicase DDX46 is involved in the epigenetic regulation of select RNA species encoding antiviral molecules, which leads to the retention of the RNAs in the nucleus and thus blockade of their translation and the activity of the proteins encoded.
Targeting the transcription factor RORγt in autoimmunity could disrupt thymocyte development and lead to thymic lymphoma. Sun and colleagues identify a two-amino-acid substitution in RORγt that ‘preferentially’ disrupts TH17 differentiation, not thymocyte development.
The effect of the cytokine IFN-λ in non-epithelial cells remains unclear. Zanoni and colleagues show that IFN-λ specifically activates a signaling pathway that diminishes the production of reactive oxygen species and degranulation in neutrophils.
The molecular events that initiate lymphoid-lineage specification remain unidentified. Cumano and colleagues define the transcriptional signatures that characterize the loss of B cell or T cell potential.
No response by an immune cell occurs in isolation but is instead the summation of multiple interacting signals. Ivashkiv and colleagues describe the epigenetic landscape that results from the integration of the inflammatory cytokines type I interferons and TNF.
Lazarevic and colleagues show that T-bet-dependent NKp46+ innate lymphoid cells reside within the meninges of the CNS and initiate meningeal inflammation, thereby facilitating T cell entry into parenchymal CNS tissues and contributing to neuroinflammation.
Immature B cells are subject to tolerance mechanisms that prevent the expression of self-reactive BCRs. Minguet and colleagues identify the membrane protein caveolin-1 as a regulator of BCR spatial organization and signaling that enforces B cell tolerance.
Specialized populations of regulatory T cells inhabit tissues and maintain homeostasis, and assist with repair functions there. Feuerer and colleagues identify a genome-wide DNA-methylation landscape to define this specialized subset of cells.
How tumors evade control by natural killer cells is ill defined. Smyth and colleagues show that natural killer cells in the tumor microenvironment can convert into type I innate lymphoid cells and intermediate type I innate lymphoid cells that favor tumor growth and metastasis.
Zhao and colleagues show that the histone lysine methyltransferase MLL4 primes the Foxp3 locus for transcriptional activation in thymus-derived and inducible regulatory T cells.
Colonna and colleagues generate mice in which both type 1 innate lymphoid cells and natural killer cells selectively lack SMAD4, which promotes canonical signaling of all cytokines of the TGF-β family. Unexpectedly, SMAD4 deficiency does not visibly affect the differentiation of type 1 innate lymphoid cells but instead alters the phenotype of conventional natural killer cells.
Previous studies have defined a state of metabolic reprogramming in rheumatoid arthritis (RA) T cells. Here Weyand and colleagues show that the rewiring of cellular metabolism renders RA T cells tissue invasive, directly promoting disease-inducing effector functions.
T cells undergo myriad changes after antigenic activation. Araki and colleagues show that CD8+ T cells exert dynamic control of mRNA translation during differentiation into effector and memory cells.
How glutamine metabolism orchestrates macrophage activation is unclear. Ho and colleagues show glutamine metabolism tailors the immune responses of macrophages through metabolic and epigenetic reprogramming.
Cathepsin S is responsible for cleaving the invariant chain Ii for the presentation of peptides by major histocompatibility complex class II on DCs. Diamond and colleagues show that the transcription factor Blimp-1 negatively regulates expression of cathepsin S and influences selection of the TFH cell repertoire and autoantibody-producing B cells.
The size of immune-cell populations needs to be tightly regulated. Shinohara and colleagues demonstrate that intracellular and secreted osteopontin control the contraction and expansion of myeloid and lymphoid populations differently under infectious and autoimmune conditions.
Liu and colleagues show that specification of the dendritic-cell lineage occurs in parallel with specification of the myeloid and lymphoid lineages in or around the hematopoietic-stem-cell stage, starting as a lineage bias defined by transcriptional programs that correlate with the combinatorial dose of IRF8 and PU.1.
Germinal centers generate high-affinity memory B cells. Qi and colleagues identify a precursor of memory B cells in germinal centers and demonstrate that the cytokine IL-9-derived from follicular helper T cells is important for their development into full-fledged memory cells.
Expression of a competent Igh heavy chain initiates a pre-BCR checkpoint during B cell development. Reth and colleagues show that protein arginine methylation by a BTG2-PRMT1 complex is required to inactivate CDK4 and thereby establish pre-B cell arrest.
Vijayanand and colleagues use genome-wide RNA sequencing for transcriptional profiling of CD8+ T cells from tumors and adjacent uninvolved lung tissue from patients with early-stage lung cancer. A tissue-resident memory signature is associated with enhanced cytotoxicity and improved survival.