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The metabolic control of B cell fate is unclear. Rickert and colleagues (p 303) show that the kinase GSK3 is a metabolic checkpoint regulator in B cells. The original image by Julia Jellusova shows a mouse spleen 7 days after immunization with sheep red blood cells. Artwork by Lewis Long.
Interleukin 1β (IL-1β) is a cytokine associated with inflammation, obesity and metabolic dysregulation. Surprisingly, IL-1β is also required for maintaining steady-state glucose homeostasis by potentiating postprandial insulin secretion.
Silencing of the chromatin remodeler Mi-2β in keratinocytes triggers local skin inflammation. Regulatory T cells activated by the cytokine TSLP control the shift from local skin inflammation to systemic lethal disease.
Elevated signaling via the metabolic checkpoint kinase mTORC1 in macrophages stimulates spontaneous granuloma formation in mice and is associated with the progression of sarcoidosis in humans.
Rosenberg and colleagues review evidence suggesting that T cells that target tumor neoantigens arising from cancer mutations are the main mediators of many effective cancer immunotherapies in humans.
Natural killer T cells (NKT cells) are thought to originate at the double-positive stage of thymopoiesis. Taniguchi and colleagues find that a subset of NKT cells also appear earlier, at the double-negative stage, and that these give rise to liver-resident NKT cells with highly potent effector function.
The cytokine IL-1β has well-established harmful effects on pancreatic islet function. Donath and colleagues identify an acute wave of postprandial IL-1β release and show that this unexpectedly has a positive effect on insulin secretion and the maintenance of normal metabolic function.
Macrophages are critical for granuloma formation, but the cell-intrinsic mechanisms remain unknown. Weichhart and colleagues demonstrate that chronic mTOR activity leads to macrophage-dependent granuloma formation, which may have relevance to sarcoidosis.
Mature B cells remain in a quiescent state until activated. Rickert and colleagues identify a prominent role for the kinase Gsk3 in resting naive B cells and in activated germinal center B cells that restrains the production of Myc and reactive oxygen species and prevents metabolic collapse.
The signaling receptor Notch is required for the generation of marginal zone B cells. Hammad and colleagues show that Notch signaling activates the kinase Taok3 and surface expression of the metalloproteinase ADAM10, which commits transitional B cells to the marginal zone B cell fate.
FcμR serves as a receptor for soluble IgM. Baumgarth and colleagues show that intracellular FcμR constrains the surface expression of IgM. Lack of FcμR alters B cell populations and enhances autoantibody production. FcμR thereby serves as a critical regulator of B cell homeostasis.
Skin is constantly exposed to environmental stressors. Georgopoulos and colleagues show that regulatory T cells respond to the cytokine TSLP produced by stressed keratinocytes and that a loss of skin Treg cell expression of TSLPR leads to lethal inflammation.
Transcription factors involved in consolidation of the induced regulatory T cell program are still being identified. Wu et al. demonstrate that the transcription factor musculin is critical for supporting the differentiation of these cells and prevents their acquisition of a T helper type 2 phenotype.
Akbar, Lanna and colleagues show that sestrin proteins bind to and coordinate the simultaneous activation of Erk, Jnk and p38 MAPKs in T lymphocytes and inhibit immunity during aging.
