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Little is known about the phosphatases involved in the control of TH17 cells. Yin and colleagues demonstrate that the phosphatase DUSP2 targets the transcription activator STAT3 to regulate the differentiation and function of TH17 cells.
The function of group 3 innate lymphoid cells (ILC3 cells) is still being determined. Vivier and colleagues describe the development of ILC3 subsets and show that NCR+ ILC3 cells are not needed to control infection with Citrobacter rodentium in the presence of an intact T cell compartment.
Mucosal surfaces often represent the first point of entry for pathogens. Paludan and colleagues demonstrate that disruption of the mucus itself can initiate a hyperacute innate immune response that precedes even the production of type I interferons.
The signals that negatively regulate group 2 innate lymphoid cells are incompletely understood. Moro and colleagues show that interferons and IL-27 restrain the function and proliferation of these cells in vitro and in vivo through a mechanism dependent on the transcription factor STAT1.
Dysregulation of group 2 innate lymphoid cells has been linked to virus-induced asthma. Fritz and colleagues demonstrate that deficiency in signaling via type I interferons in these cells can lead to dysregulated type 2 immunity during respiratory viral infection.
Group 3 innate lymphoid cells have low expression of the transcription factor GATA-3. Zhu and colleagues show that despite its low expression, GATA-3 is essential for the homeostasis, further maturation and effector function of lineage-committed group 3 innate lymphoid cells.
Proteomic profiling can provide new insight into the cellular regulation of effector functions. Cantrell and colleagues report discordant mRNA profiles and protein profiles in activated CD8+ T cells and reveal new roles for mTORC1 in regulating the function of cytotoxic T lymphocytes.
Memory TH2 cells are rapidly recruited to tissues after exposure to stimulatory ligands. McKenzie and colleagues demonstrate that ILC2s have an essential role in facilitating TH2 cell memory responses in lung, skin and gut.
Glucose availability is limiting in tumor environments. Zou and colleagues show that reduced glycolytic metabolism in T cells within tumors suppresses expression of the methyltransferase EZH2, which limits production of antitumor effector molecules and enhances T cell apoptosis.
The TCR-peptide-MHC interface is composed of conserved and diverse regions, but the relative contributions of each in shaping T cell recognition remain unclear. Garcia and colleagues show consistent germline interactions between TCR and MHC, but enough flexibility in the TCR-peptide-MHC interface to allow adjustment for different peptides.
The mechanisms that regulate the tissue-specific localization and functions of innate lymphoid cells are poorly understood. Xiong and colleagues find that CCR10+ innate lymphoid cells are selectively programmed in skin-draining lymph nodes for cutaneous homeostatic regulation.
Mitochondria can contribute to an increase in the amount of phagosomal reactive oxygen species and thereby promote the effective killing of bacteria. Study of mice deficient in Mst1 and Mst2 reveals a role for these kinases in recruiting mitochondria to phagosomes.
Docking of T cell antigen receptors (TCRs) engaging complexes of peptide and major histocompatibility complex has shown the same diagonal orientation and polarity. A new study demonstrating that TCRs from regulatory T cells bind with reversed polarity challenges this dogma.
The TH17 subset of helper T cells drives emphysema in smokers, but how these cells are elicited remains unknown. A study now links the microRNA miR-22 and the histone deacetylase HDAC4 to regulation of the activation of antigen-presenting cells after exposure to smoke.