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Obesity is often accompanied by chronic inflammation. Li and colleagues show that, in mice fed high-fat diets, IL-1 signaling in adipocytes induces an unconventional IRAK2 translocation to mitochondria and suppresses respiratory super-complex formation to alter mitochondrial function, and exacerbates obesity.
Autophagy controls cellular homeostasis and influences immune responses. Galluzzi and colleagues show that tumor cell autophagy opposes inflammatory cell death following radiation therapy and can be inhibited to enhance antitumor responses.
The CTLA-4–Ig fusion protein (abatacept) can have beneficial effects in autoimmune disease. Walker and colleagues show in mouse and human type 1 diabetes that abatacept targets pathogenic follicular helper T cells, and the frequencies of these cells at baseline can be used to stratify treatment responses in patients.
Pathological group 2 innate lymphoid cells (ILC2s) have mainly been implicated in allergy. Halim and colleagues demonstrate that ILC2s orchestrate a prometastatic pathway via the recruitment of eosinophils that suppress NK cell function.
Banchereau and colleagues provide a resource dataset that examines disease-related transcriptional profiles of peripheral whole-blood cells from adolescent patients with SLE by single-cell RNA-seq analysis.
Kim and colleagues provide new insights into the function and fate of neutrophils during influenza infection and their roles in antiviral T cell responses.
The epigenetic landscape of human αβ and γδT cell development has remained unexplored thus far. Taghon and colleagues provide a resource of RNA-seq and ATAC–seq profiles examining human thymocyte development.
Luo and colleagues use single-cell RNA sequencing to provide a comprehensive transcriptional landscape of neutrophil maturation, function and fate decision in their steady state and during bacterial infection.
Verykokakis and colleagues show that the transcription factor BCL-6 is highly expressed in stage 0 NKT and is absolutely required for innate T cell lineage development. BCL-6 acts to modify the chromatin landscape and is needed to promote the ST0–ST1 transition and PLZF expression.
STING ER exit is the rate-limiting step in STING signaling, but the mechanism that drives this process is not understood. Paludan and colleagues identify CxORF56, called STEEP here, as a positive regulator of STING signaling.
Plasmacytoid dendritic cells (pDCs) are a major source of type I interferon (IFN-I). Dalod and colleagues show that IFN-I production and T cell activation were performed by the same pDC, but these occurred sequentially and in different micro-anatomical locations during virus infection.
How Lck is recruited to the TCR to initiate signaling is not well known. Here Minguet and colleagues report a previously unknown binding motif in the CD3ε cytoplasmic tail that interacts in a noncanonical mode with the Lck SH3 domain that may help to improve TCR activation and the antitumor activity of a clinically approved CAR.
T cell exhaustion limits antitumor immune responses. Vignali and colleagues identify neuropilin-1 as a novel immune checkpoint that cell-intrinsically operates to limit memory cell formation and can be targeted to enhance antitumor responses.
Gilliet and colleagues demonstrate that skin wound healing occurs through the coordinated action of plasmacytoid dendritic cells, chemokines and skin microbiota.
Thompson and colleagues show that repetitive antigenic stimulation within the tumor environment triggers mitochondrial dysfunction by inhibiting oxidative phosphorylation, which leads to T cell exhaustion.
Van Gisbergen and colleagues show that tissue-resident memory T cells, genetically marked in Hobit reporter mice, can exit tissues upon reinfection and contribute to systemic memory responses.
Geiger and colleagues use SILAC and mass spectrometry to study protein turnover in human T cells and examine how naive T cells maintain their quiescence and transition to activated cells.
Huppa and colleagues highlight signaling deficiencies in chimeric antigen receptor (CAR)-modified T cells that limit the efficacy of CAR T cell therapies to target tumors with diminished antigen expression.
Takayanagi and colleagues show that the chromatin remodeler Chd4 works with both Fezf2 and Aire to promote promiscuous tissue-restricted antigen expression in medullary thymic epithelial cells, mediating central tolerance in the thymus.
Familial Mediterranean fever is an autoinflammatory disease caused by gain-of-function mutations in the pyrin inflammasome. Kastner and colleagues show that mutant pyrin better resists suppression by the plague bacterium Yersiniapestis and may have been positively selected in human Middle Eastern populations.