Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Transdifferentiation between group 1 and group 3 innate lymphoid cells (ILCs) has been observed in the gut. Spits and colleagues now show lung ILC2s are able to convert into ILC1s in an IL-12-dependent manner.
Xue and colleagues show that the transcription factors Tcf1 and Lef1 suppress CD4+ T lineage genes in CD8+ T cells through intrinsic histone deacetylase (HDAC) activity.
Intracellular proteins are regulated by multiple post-translation modifications. Cantrell and colleagues show that nutrient flux regulates intracellular protein modification by O-GlcNAcylation, which drives thymocyte development and T cell proliferation.
Group 1 and 3 innate lymphoid cells can be functionally plastic. Humbles and colleagues find that group 2 innate lymphoid cells in the lungs also exhibit phenotypic plasticity after exposure to infectious or noxious agents.
Cytokines of the IL-1 family have a range of effects on innate lymphoid cells. Liu and colleagues find that IL-1 facilitates the maturation and plasticity of group 2 innate lymphoid cells.
Moore and colleagues show that Mycobacterium tuberculosis induces miR-33 and miR-33* in macrophages to inhibit integrated pathways involved in autophagy, lysosomal function and fatty acid oxidation, and to support bacterial replication.
Invariant natural killer T cells recognize lipid antigens presented by CD1d molecules and are capable of copious cytokine production. Kronenberg and colleagues show that distinct transcriptional and epigenetic profiles can be ascribed to the NKT1, NKT2 and NKT17 subsets of these cells.
The aryl hydrocarbon receptor (AHR) has well-described roles in the differentiation of T cells; however, less is known about its function in innate immunity. Takaoka and colleagues demonstrate how an AHR-dependent pathway reins in production of type I interferon.
Asymmetric division can generate effector and memory CD8+ T cell precursors. Powell and colleagues show asymmetric partitioning of mTORC1 activity upon CD8+ T cell division, which results in distinct metabolic programming of daughter T cells.
The physiological function of the mammalian chitinase AMCase is unclear. Wynn and colleagues show that it is dispensable for allergic lung inflammation but is necessary for clearance of intestinal helminths.
The cell-intrinsic pathways controlling the function of innate lymphoid cells are poorly defined. Artis and colleagues demonstrate that ILC2s selectively express arginase 1 and that this is critical for their bioenergetics, proliferation and function.
Positively selected thymocytes require a maturation phase before emigrating from the thymus. Hogquist and colleagues show that functional maturation is driven by tonic signals provided by type I interferons and the transcription factor NF-κB.
Activation of the transcription factor IRF3 is a key event in antiviral responses. Lichty and colleagues show that recruitment of the mTOR downstream effector S6K1 to the STING-TBK1 signaling complex is required for the activation of IRF3 after infection with DNA viruses.
Using single-cell transcriptome profiling of pre-granulocyte-macrophage progenitor cells, Nerlov and colleagues identify an early hematopoietic lineage bifurcation that segregates mast cells, eosinophils, megakaryocytes and erythroid cells from monocytes, neutrophils and lymphocytes.
MR1 molecules present bacterial metabolites to MAIT innate lymphocytes, but the processing and presentation pathway of these ligands are unclear. McCluskey, Rossjohn, Villadangos and colleagues demonstrate that MR1 ligands bind in the ER, which initiates trafficking to the plasma membrane and subsequent presentation.
The thymus produces γδ T cell subsets making either IFN-γ or IL-17. Silva-Santos and colleagues show that TCR signal strength within specific developmental windows is a major determinant of the generation of these γδ T cell subsets.
The causative mechanism for the immunodeficiency and autoinflammatory disease XLPDR is unknown. Burstein and colleagues show that XLPDR is caused by disruption of POLA1, which encodes a DNA polymerase subunit; this, in turn, leads to dysregulated production of type I interferons.
The subsets of antigen presenting cells (APCs) that mediate tolerance to oral antigens remain unclear. Mucida and colleagues use lineage-specific depletion of APCs to show that monocyte-derived APCs are dispensable, while classical dendritic cells are critical, for the induction of regulatory T cells and oral tolerance.
Inflammasome activation triggers the release of active interleukin 1β (IL-1β). Li and colleagues show that TH17 cells can release IL-1β upon T cell antigen receptor and ATP stimulation via an ASC–NLPR3–caspase-8 axis, thereby contributing to neuroinflammation.
14-3-3ɛ serves a crucial function in antiviral immunity by mediating the translocation of RIG-I from the cytosol to mitochondria. Chan and Gack have found that the NS3 protein of Dengue virus binds to 14-3-3ɛ via a highly conserved phosphomimetic motif and thereby blocks RIG-I translocation and antiviral signaling.