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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.
The resolution of inflammation is a protective response. The identification and characterization of new players that boost this response might inform the development of novel therapies for non-resolving inflammatory diseases.
Epelman and colleagues use fate mapping and single-cell transcriptomics to describe the dynamics of resident and recruited cardiac macrophages during ischemic injury.
While important evidence for the role of myeloid cells in myocardial infarction has accumulated in recent years, single-cell transcriptomics fully delineates the functional heterogeneity of the myeloid cell compartment.
Yu and colleagues show that the transcription factor XBP1s positively regulates the cytolytic activity of human NK cells and is required for the IL-15-mediated survival of NK cells.
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.