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The contribution of innate lymphoid cells (ILCs) to immunity in natural conditions is unclear. By studying circulating and tissue-resident ILCs in patients with severe combined immune deficiency, Vély and colleagues (p 1291; News and Views by Le Gros et al. p 1237) show that ILCs are dispensable for immunological protection in the context of modern medicine and hygiene. The original image by Julie Bruneau shows scattered NKp46+ ILCs (brown) in the lamina propria and T cells (red) in the epithelium of a colonic biopsy. Artwork by Lewis Long.
A cohort of immunodeficient children lead near-normal lives after bone marrow transplantation, despite a profound deficiency of innate lymphoid cells (ILCs).
By taking advantage of an MR1 tetramer to accurately detect mucosal-associated invariant T (MAIT) cells in both mice and humans, researchers defined the thymic development of MAIT cells.
Microglia are important facilitators of glioma proliferation and invasion. An important component of this process seems to be glioma-mediated suppression of microglial activation via S-nitrosylation of microglial caspase-3.
Epithelial cells of the gut are heavily glycosylated. Kiyono and colleagues review the evidence for the importance of this glycosylation to immunity, host–microbiome interactions and immunopathology.
tRNA synthetases are essential to protein synthesis. Kim and colleagues identify a non-translational function for glutamyl-prolyl-tRNA synthetase during viral infection that promotes the anti-viral activity of the antiviral signaling protein MAVS.
Cybulsky and colleagues show that myeloid cells in the arterial intima undergo reverse transendothelial migration into the arterial circulation that is dependent on the chemokine CCL19 and its receptor CCR7.
Tumor cells commonly express abnormally glycosylated glycoproteins such as MUC1. Burchell and colleagues show that tumor-specific MUC1-ST interacts with the lectin Siglec-9 on myeloid cells and induces their conversion into suppressive tumor-associated macrophages.
Gliomas recruit and manipulate microglial function to promote their growth. Joseph and colleagues reveal the molecular basis of this manipulation by showing that gliomas trigger S-nitrosylation of microglial caspase-3 and thereby initiate a tumor-promoting phenotype.
The importance of human innate lymphoid cells to normal human physiology is unclear. Vivier and colleagues find that immunodeficient patients ‘rescued’ with normal bone marrow can recover their T cells but not their innate lymphoid cells, yet remain entirely asymptomatic for nearly 40 years.
Godfrey, Pellicci and colleagues define the developmental stages and checkpoints for the development of mucosal-associated invariant T cells in humans and mice.
The longevity of hematopoietic stem cells requires strict regulation to prevent their exhaustion. Aifantis and colleagues show that the ubiquitin E3 ligase Huwe1 is needed to suppress the activity of the transcription factor N-myc and maintain the quiescence and function of these cells.
The cytokine receptor IL-2R is essential for the development of Treg cells; therefore, it has been difficult to separate this from its role in the suppressive function of Treg cells. Rudensky and colleagues use various genetic systems to show that capture of IL-2 by IL-2R is important for suppression of CD8+ T cells but not that of CD4+ T cells.