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Open conformers of the non-classical and monomorphic major histocompatibility complex (MHC) class I molecule HLA-F are ligands for the activating receptor KIR3DS1 and trigger the activation of natural killer (NK) cells.
At least five recent papers have shown an unexpected antigenic relationship between Zika and dengue viruses, with potential implications for vaccines and therapeutics.
There is now a major effort to fully exploit the anti-tumor properties of NK cells in the clinic. In this Review, Smyth and colleagues detail recent advances in NK cell–based immunotherapies and discuss the advantages and limitations of these strategies.
The thymic development of CD8+ T cells requires the presentation of different sets of peptides on major histocompatibility complex class I for positive selection and negative selection.
The Pyrin inflammasome guard is disabled if the activity of small cellular GTPase is compromised in response to defects in the mevalonate pathway and is disabled directly by mutations in the gene encoding Pyrin, which results in the interleukin 1β (IL-1β)-driven autoinflammatory diseases MKD and FMF.
The E3 ubiquitin ligase Itch limits interleukin 17A (IL-17A)-mediated intestinal inflammation by targeting the transcription factor ROR-γt for proteasomal degradation.
Induction of the transcription factor Bcl11b in early T cell precursors is supported by three positive forces: signaling via the transmembrane receptor Notch1 provides stochastic permissivity; the transcription factors TCF-1 and GATA-3 poise the locus for expression; and the transcription factor Runx1 steps in to raise expression.
IL-1α is a ubiquitously expressed cytokine that has diverse roles in immunity and homeostasis. Di Paolo and Shayakhmetov review IL-1α's distinctive and important role in inflammation.
In natural killer (NK) cells, CIS restrains a signaling pathway elicited by interleukin 15 (IL-15) that leads to activation of the kinase JAK1. Removal of CIS from NK cells increases their capacity to reduce the metastatic dissemination of breast cancer and melanoma in mice.
B cell and T cell memory differentiation requires the transcription factor Bach2, which inhibits the effector-cell fate by limiting antigen-receptor-stimulation-induced gene expression and restricting premature expression of the transcriptional regulator Blimp-1.
Perivascular and subdural meningeal macrophages at the interface between the central nervous system and the periphery are self-renewing and arise from early embryonic precursors. Macrophages residing in the choroid plexus have dual origin, developing from circulating bone-marrow-derived monocytes and embryonic progenitors.
The appearance of innate lymphoid cells was a major step in the evolution of vertebrate immunity. In their Perspective, Vivier et al. survey these cells in evolution and their functional inter-relationship with conventional T cells and B cells.
Innate lymphoid cells (ILCs) arise from distinct hematopoietic progenitors. Zook & Kee discuss the transcriptional programs that direct the development of natural killer cells and various ILC subsets.
In this Review, Klose and Artis focus on how group 2 ILC and group 3 ILC responses are regulated and how they interact with other immune and non-immune cells to mediate their functions.
NK cells and ILC1s are developmentally distinct but share many functional similarities. Spits and colleagues describe current knowledge on the biology of these cells and the conditions under which they can be distinguished.
The redundant or specialized roles of innate lymphoid cells (ILCs) relative to those of T cells in vivo remain hard to delineate experimentally. Bando and Colonna review the current understanding of the specialized in vivo functions of ILCs and discuss the genetic mouse models used to assess the contributions of ILCs versus those of T cells.
Tissue-resident innate lymphoid cells (ILCs) perform diverse roles in regulating mucosal homeostasis and inflammation. The transdifferentiation of ILC2s into interferon-γ (IFN-γ)-producing ILC1-like cells generates a highly inflammatory immune cell.
The transcription factors Tcf1 and Lef1 have intrinsic histone-deacetylase activity that is required for the repression of CD4+ T cell–lineage genes in CD8+ T cells.
