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RNAs can be dynamically modified by N6-methylation of adenosine (m6A), which leads to their destabilization. Stern-Ginossar and colleagues demonstrate a role for m6A modification of host transcripts encoding type I interferons during viral infection.
Epelman and colleagues use fate mapping and single-cell transcriptomics to describe the dynamics of resident and recruited cardiac macrophages during ischemic injury.
Germinal center B cells undergo reiterative rounds of proliferation and selection. Melnick and colleagues show that the histone demethylase LSD1 is necessary for this reiterative process via its interactions with the transcription factor BCL6.
Tissue-resident memory cells are functionally distinct from lymph node memory cells. Randall and colleagues show that lung infection establishes B cell memory in situ and confers superior responses following challenge infection, which will inform vaccine design for respiratory viruses.
Li and colleagues show that G3BP1, a protein known to regulate the RNA stress response, is critical for DNA sensing and efficient activation of the cytoplasmic DNA sensor cGAS.
Macrophages alter their metabolism in response to infection. The authors show that resting macrophages generate nicotinamide adenine dinucleotide via de novo synthesis, but activated and aged cells suppress the rate-limiting enzyme quinolinate phosphoribosyltransferase to regulate mitochondrial and immunological functions.
DEL-1 protein interferes with leukocyte adhesion to prevent inflammation. Chavakis and colleagues now show that DEL-1 contributes to tissue resolution after inflammation by promoting macrophage-mediated efferocytosis and M2-like pro-resolving activities.
Yarovinsky and colleagues identify the alarmin S100A11, which is released from Toxoplasma gondii–infected cells, as the trigger for immune responses in humans. S100A11 induces expression of the chemokine CCL2, which recruits inflammatory CCR2+ monocytes to the sites of infection.
Hayday and colleagues show that the responsiveness of mouse and human γδ IELs to Btnl or BTNL proteins is mediated by germline-encoded motifs within the cognate TCR Vγ chains, while Vγ chain motifs generated by somatic gene rearrangement remain available for nominal antigen binding.
Obesity is a risk factor for cancer. Lynch and colleagues show that obesity alters the cellular metabolism of natural killer cells and decreases their antitumor surveillance and effector responses.
Thymocyte development requires a complex orchestration of multiple transcription factors. Gournari and colleagues find that Tcf-1 and HEB cooperate to establish the epigenetic and transcription profiles of CD4+CD8+ thymocytes
Tumors can vary in both their control by immunosurveillance and their glycolytic activity. Bopp and colleagues demonstrate that highly glycolytic tumors acidify their microenvironment and use this to initiate a mechanism of localized immunosuppression.
Endosomal TLR4 signaling activates type I interferons via a TRIF-dependent pathway. Vogel and colleagues identify autocrine production of PGE2–EP4–cAMP as a negative regulator of the TRIF pathway that suppresses IFN-β expression induced by Gram-negative bacteria.
Treg cells are essential for enforcing peripheral tolerance but can also influence tissue regeneration. Afzali and colleagues use high-dimensional analysis to describe a distinct population of CD161+ human Treg cells involved in wound healing of the intestinal mucosa.
Pneumococcal carriage in the upper respiratory tract is an important determinant of influenza severity. Jochems et al. use human systems analysis to show that influenza-induced inflammation increases bacterial burden in the nasal cavity with implications for secondary bacterial pneumonia.
Regulatory T cells (Treg cells) can destabilize in inflammatory environments. Sumida et al. show that β-catenin signaling perturbs Treg cell function in patients with multiple sclerosis and under experimental high-salt conditions.
LAG-3 is a co-inhibitory receptor on T cells, but its mode of action is controversial. Okazaki and colleagues demonstrate that LAG-3 preferentially binds stable MHC class II complexes and thereby selectively maintains tolerance of self-reactive T cells.