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Shemesh et al. report that the development of FcRγ−/low adaptive-like NK cells requires reduced mTOR activity and depends on TGF-β or IFN-α.

Reviews

Innate lymphoid cells are critical for tissue protection and immunity in animals, and their localization at the body’s surfaces position them to respond rapidly. Yu and colleagues review the metabolic pathways that underlie ILC phenotype and function and adaptation to dynamically changing conditions for homeostasis.

Brief Definitive Reports

In Special Collection: Tolerance and Autoimmunity

The EBV-specific T cell receptor repertoire is broader in multiple sclerosis patients, even in diseased siblings of discordant monozygotic twin pairs, indicating an ongoing immune response to Epstein–Barr virus in multiple sclerosis patients, which might hold clues for multiple sclerosis pathogenesis and future therapeutic or preventive avenues.

Technical Advances and Resources

Using a multi-omics approach, this study provides a comprehensive database in humanized APOE4 transgenic mice showing dysregulated signaling mechanisms in endothelium and pericytes that reflect a molecular signature of a progressive blood–brain barrier failure that precedes synaptic dysfunction and behavioral deficits.

Articles

Diminished human NK cell proliferation limits FcεRIγ expression, leading to an adaptive-like NK cell phenotype, and may have an early prognostic value for COVID-19 disease severity, associated with increased inflammation and higher TGFβ and IFNα levels.

ILC3s are crucial for the maintenance of host–microbiota homeostasis in gastrointestinal mucosal tissues. This study shows that BATF globally shapes the chromatin landscape of intestinal ILC3s, which in turn orchestrates microbiota and mucosal CD4+ T cell immunity.

The chronic activation of pDCs is a key feature in multiple autoimmune diseases. This article reports that pDCs from autoimmune patients have defects in the regulation of metabolic pathways and that blocking the TCA cycle abrogates chronic IFN-I responses.

In an international cohort of 279 patients with hypoxemic influenza pneumonia, we identified 13 patients (4.6%) with autoantibodies neutralizing IFN-α and/or -ω, which were previously reported to underlie 15% cases of life-threatening COVID-19 pneumonia and one third of severe adverse reactions to live-attenuated yellow fever vaccine.

Tissue necrosis is a major pathophysiological hallmark of disease progression in tuberculosis. In this study, Amaral et al. show that GPX4, an antioxidant selenoenzyme, is an essential regulator of both lipid peroxidation–mediated cellular necrosis and host resistance in Mycobacterium tuberculosis infection.

Sleep interruption restructures the epigenome of hematopoietic stem and progenitor cells (HSPCs) and increases their proliferation, priming them for exaggerated inflammatory bursts and reducing hematopoietic clonal diversity through accelerated genetic drift. In humans, sleep restriction alters the HSPC epigenome and activates hematopoiesis.

In Special Collection: Hematology 2022

Heparan sulfate (HS) glycotyping establishes a role for HS modification patterns in hematopoietic lineage differentiation in mouse and human, and provides an orthogonal approach to define and isolate viable cell types across different lineages and species.

In Special Collection: Hematology 2022

B lineage transcription factor EBF1 is expressed at low levels in MPP3 and MPP4 cells. EBF1 primes the chromatin of B-lymphoid enhancers in MPP3 cells, and hematopoietic Ebf1 deletion results in augmented C/EBPα-target gene signature and enhanced myeloid differentiation.

In Special Collection: Hematology 2022

Mitigation of treatment-induced thrombocytopenia is an unmet clinical need in patients with myelodysplastic syndrome or acute myeloid leukemia undergoing azacitidine therapy. Okoye-Okafor et al. uncover mechanistic drivers of AZA-induced platelet production impairment, which can be counteracted therapeutically.

Chaves-Pérez et al. report mechanisms of regulation of ISC proliferation following injury. The death of transit-amplifying cells triggers inflammation that reduces R-spondin production within the crypt, thereby abolishing ISC proliferation. Transit-amplifying cells represent a cellular platform modulating inflammatory responses to control ISC proliferation and tissue regeneration.

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