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TET proteins regulate 5-methylcytosine epigenetic marks, and thereby regulate chromatin accessibility. Rao and colleagues show that the combined loss of TET2 and TET3 in thymocytes skews development to iNKT17 cells as a result of upregulation of RORγt, which leads to lymphoproliferative disease and premature death.
Notch signaling promotes the maintenance of lung-resident CD8+ memory T cells that are transcriptionally poised for rapid effector responses but have heightened expression of inhibitory receptors, suggestive of tight regulation.
Deficiency in the RASGRP1 guanine-nucleotide-exchange factor leads to a novel primary immunodeficiency with impaired activation and proliferation of T cells and B cells and defective killing by cytotoxic T cells and natural killer cells.
Natural killer cells are a rapid source of the cytokine IFN-γ that influences ensuing immune responses. Schwab and colleagues report that gradients of the signaling lipid S1P regulate the positioning of natural killer cells in lymph nodes necessary for this response.
Krönke and colleagues show that the cytokine IL-23 controls the glycosylation profile and inflammatory activity of autoantibodies through control of sialyltransferase activity in plasma cells mediated by the TH17 subset of helper T cells.
Lymphocytes integrate multiple input signals to regulate the extent of their proliferative response. Hodgkin and colleagues demonstrate that the proto-oncoprotein Myc is a cell-intrinsic division timer.
The cytokine IL-18 can drive autoantibody production. Karlsson and colleagues show that such responses are limited by a three-way cellular interaction whereby splenic neutrophils activate both B cells and invariant natural killer T cells but the activated B cells are killed by FasL+ invariant natural killer T cells.
Fibroblastic reticular cells influence the function of lymphocytes in secondary lymphoid organs. Ludewig and colleagues demonstrate that they also specifically restrain the activation of group 1 innate lymphoid cells in the presence of microbial stimulation to prevent immunopathology.
Knapp and colleagues show that elevated heme levels following hemolysis impair the control of bacterial proliferation by inhibiting phagocytosis and migration of human and mouse phagocytes independently of heme-iron acquisition by bacteria as a source of nutrients.
T follicular helper (TFH) cells are important for the formation of germinal centers and antibody responses. Kubo and colleagues show that TH1 cells can induce a protective antibody response in the complete absence of TFH cells and germinal centers.