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.
TH9 cells secrete copious amounts of IL-9, but how their generation is controlled remains poorly defined. Li and colleagues demonstrate that ligation of the costimulatory receptor OX40 potently generates TH9 cells in a manner dependent on noncanonical NF-κB signaling.
Natural killer T cells (NKT cells) recognize lipid antigens presented by CD1d. Zajonc and Rossjohn and their colleagues describe molecular interactions between type II NKT cell antigen receptors and CD1d-ligand complexes, which demonstrate distinct modes of recognition used by the receptors.
Natural killer T cells (NKT cells) recognize lipid antigens presented by CD1d. Zajonc and Rossjohn and their colleagues describe molecular interactions between type II NKT cell antigen receptors and CD1d-ligand complexes, which demonstrate distinct modes of recognition used by the receptors.
Lyl-1 is a transcription factor expressed in hematopoietic progenitors. Goodell and colleagues show that Lyl-1 is required for lymphoid specification and the maintenance of early T lineage progenitors.
The mechanisms of TGF-β-mediated inhibition of TH2 differentiation remain unclear. Nakayama and colleagues show that TGF-β induces the transcription factor Sox4, which negatively regulates the transcription factor GATA-3 by two independent mechanisms.
TCR microcluster signaling occurs in cognate T cells after they encounter antigen-presenting cells. Krummel and colleagues show that immune synapses are motile as microclusters coalesce after the actin depolymerization that occurs during T cell movement.
IL-2 production is actively suppressed during TH17 differentiation. Quintana and colleagues show that the transcription factor Aiolos is induced by the transcription factors STAT3 and AhR and silences the Il2 locus.
Tissue-specific Langerhans cells and microglia develop in situ before birth. Colonna and colleagues identify IL-34 produced by keratinocytes and neurons as the relevant ligand of CSF1R necessary for their generation.
Hair is a skin component that functions as a physical barrier and thermal regulator. Nagao and colleagues show that hair follicles recruit Langerhans cells to the epidermis via the secretion of various chemokines.
Fusion with the cell membrane is the earliest event in viral infection. Paludan and colleagues show that 'unscheduled' membrane-fusion events elicit an innate immune response dependent on the adaptor STING.
Intestinal microfold (M) cells actively capture luminal antigens and move them by transcytosis to initiate immune responses. Ohno and colleagues show that the Ets transcription factor Spi-B is necessary for M-cell differentiation.
The functional basis of elite control of HIV is still unclear. Walker and colleagues show that elite controllers are tolerant of viral escape variants and more rapidly mobilize cytotoxic granules to the immunological synapse.
Tetramers of peptide and major histocompatibility complex (pMHC) are very useful for the detection of specific T cell antigen receptors; however, they have several drawbacks. Davis and colleagues describe photocrosslinkable pMHC monomers with several important advantages and use these to probe the immunological synapse.
Little is known about the regulation of the ST2L receptor for IL-33. Zhao and colleagues identify the F-box protein FBXL19 as being key to the degradation and negative regulation of ST2L.
In lymph nodes, cellular positioning can dictate the immune response. Lund and colleagues show that nematode infection triggers interactions between lymphotoxin-producing B cells and CXCR5+ dendritic cells and CD4+ T cells to initiate T helper type 2 responses.
The pleiotropic cytokine TGF-β is involved in the generation of Treg cells and maintaining tolerance. Zhang and Bevan show that TGF-β acts specifically to block the proliferation of low-affinity T cells independently of effects on the development of Treg cells.
Whether cross-interference between innate immune receptors affects the outcome of immune responses remains unclear. Taniguchi and colleagues show that RLR activation interferes with activation of the Il12b promoter induced by TLR signaling.
Notch signaling is known to modulate macrophage polarization. Hu and colleagues show that the Notch–RBP-J axis controls the expression of M1 macrophage–specific genes by promoting translation of the transcription factor IRF8.
Dock8 deficiency leads to defects in humoral immunity. Geha and colleagues show that Dock88 interacts with MyD88 to bridge TLR9 signaling to the Src-Syk-STAT3 pathway to promote B cell proliferation and differentiation.
Activated B cells can tailor their ensuing antibody responses by isotype switching. McHeyzer-Williams and colleagues demonstrate B cell–intrinsic requirements for the transcription factors T-bet and RORα in maintaining IgG2a+ and IgA+ memory cells, respectively.