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M cells are intestinal epithelial cells specialized for sampling bacterial antigens. Takayanagi and colleagues (p 675; News and Views by Belz and Almeida p 601) show that previously unknown mesenchymal cells expressing the cytokine RANKL induce M cell differentiation. The original scanning-electron-microscopy image by Kazuki Nagashima shows an M cell taking up three bacteria in Peyer's patches. Artwork by Lewis Long.
RNA-binding proteins (RBPs) take control of binary cell-fate 'decisions' and cellular identity in lymphoid organs, as the RBP ZFP36L1 is shown to negatively regulate the stability of the transcription factors KLF2 and IRF8 to control the maintenance, survival and localization of marginal zone B cells.
The transcription factor STAT5 acts as an oncoprotein in B cell acute lymphoblastic leukemia, competing with the transcription factors NF-κB and Ikaros for binding to DNA.
Monocytes recruited to the peritoneum under conditions of a type 2 inflammatory reaction can convert into resident-type macrophages under the control of vitamin A.
M cells sample gut lumenal antigens and microbes to induce gut immune responses. A novel population of stromal cell—the M cell inducers—are essential for sustaining M cell differentiation and bacteria-specific production of immunoglobulin A to maintain the gut–immune system symbiosis.
Although interleukin 17 (IL-17) has modest activity on its own, it has a substantial impact in immunity through its synergistic action with other factors and its self-sustaining feedback loop. Veldhoen discusses the role of IL-17 during infections.
Neonates are thought to have impaired immune responses, yet, paradoxically, they can also demonstrate hyperinflammation. Ulas et al. show that a neonatal burst of the alarmins S100A8 and S100A9 activates a distinct innate immune response without dangerous hyperinflammation.
Microglia are the tissue-resident macrophages of the brain. Ouyang and colleagues show the ER-resident transmembrane protein NRROS is necessary for proper development and function of microglia. Mice lacking NRROS exhibit neurologic defects and die prematurely.
Loke and colleagues show that vitamin A is required for the conversion of interleukin 4 (IL-4)-activated monocyte-derived macrophages into macrophages with a tissue-resident phenotype in the peritoneal cavity and in S. mansoni–induced liver granulomas in mice.
Obesity is commonly accompanied by inflammatory responses in white adipose tissues. Chavakis and colleagues identify a vicious cycle involving α4 integrins and the adhesion molecule VCAM-1 that promotes inflammatory macrophage–adipocyte interactions and suppresses beige adipogenesis.
Macrophages serve important functions in defense and tissue homeostasis. Jung and colleagues demonstrate that a resident population of macrophages controls the innervation of brown adipose tissue and thereby regulates energy use.
IgA is necessary for maintaining gut homeostasis, and its production depends on microbial sampling by the gut-associated lymphoid tissue (GALT). Takayanagi and colleagues identify a novel population of mesenchymal cells in the GALT that control M cell differentiation and function of gut epithelium.
Turner and colleagues show that the RNA-binding protein ZFP36L1 regulates a post-transcriptional hub that determines the identity of marginal-zone B cells by promoting their localization and survival.
Transcription factors compete for superenhancer sites and have antagonist functions. Farrar and colleagues identify regulatory competition between STAT5 and IKAROS or NF-κB in B cells and show that the ratio of STAT5 to IKAROS or to NF-κB can serve as a prognostic marker of disease severity of the leukemia B-ALL.