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Neutrophils can release S100A8/S100A9 as an alarmin via gasdermin D pores. Here, the authors untangle the regulatory mechanisms driving this pathway and show that active repair processes make these pores transient, which can prevent the usual lytic cell death.
Iliev et al. report that increased Candida albicans accumulation in the mycobiota of patients with severe COVID-19 might be a contributing factor to the immunopathology of severe COVID-19 and have long-lasting effects on the hematopoietic stem cell compartment.
Einav and colleagues characterize peripheral immune blood cells from pediatric patients with severe natural dengue infections. Their findings suggest that disease progression is associated with an inflammatory phenotype accompanied by impaired interferon response, defective antigen presentation and regulation of effector lymphocyte responses.
Liu and colleagues find differential effects of microglial apoE isoforms on brain function and microglial responses. ApoE3 enhances microglial responses, promoting brain function and reducing amyloid deposition and associated neurotoxicity, while the Alzheimer’s disease-associated apoE4 results in lipid droplet accumulation and impaired microglial responses, which are critical for limiting the development of amyloid pathology.
Using TEA-seq, Thomson et al. detail transcriptional and epigenetic alterations in the T cell compartment between healthy children and older adults, leading to the discovery of a novel pediatric CD8αα+ population poised for rapid effector responses.
Eisenlohr and colleagues identify a novel influenza A virus peptide that elicits a robust CD8+ T cell response and is restricted by the nonclassical Qa-1 class I molecule.
Here, the authors show that deletion of Pglyrp1 promotes antitumor immunity owing to its inhibitory function in CD8+ T cells and that targeting it can inhibit development of autoimmune neuroinflammation. These findings indicate that PGLYRP1 might be a target for immunotherapy.
Yuan and colleagues show that ERMAP expression on cancer cells delivers an ‘eat me’ signal to Kupffer cells by binding to Gal-9–dectin-2 on Kupffer cells and triggering phagocytosis.
The malate shuttle is understood to control the NAD+/NADH balance. Here the authors show that GOT1, a central enzyme in the malate shuttle, rather promotes antiviral CD8+ T cell responses by detoxifying ammonia.
Peduto and colleagues report a role for ADAM12+ mesenchymal stromal cells at the tumor margins and their interaction with immune cells to promote a permissive ‘protumor’ environment.
The APOE4 allele is a major genetic risk factor for the development of late-onset Alzheimer’s disease (AD). In this manuscript, Butovsky and colleagues suggest that APOE4 impairs the microglial response in AD by inducing TGFβ-mediated checkpoints.
Here the authors use single cell profiling of T cells across the human lifespan to show that a suboptimal TCR shift in T cells as we enter older age results in a molecular signature that resembles that of T cells from newborns and children.
Satija and colleagues use multimodal sequencing technologies and cross-modality integration tools to define distinct subpopulations of CD8+ T cells that are predictive of COVID-19 severity.
Wherry and colleagues define the kinetics of vaccine-primed recall immune responses during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) breakthrough infection, highlighting rapid activation of memory T cells and broadly enhanced immune responses in previously vaccinated individuals.
The mechanisms by which noncoding genetic variation shapes tissue macrophage phenotypic diversity remain obscure. Glass and colleagues define cell-intrinsic and environmental effects contributing to genetic control of Kupffer cell transcription.
Verdeil and colleagues show that the transcription factor NFAT5 is selectively required in tumor-induced, but not chronic infection-induced, CD8+ T cell exhaustion, possibly due to the modulation of NFAT5 activation by hyperosmolarity in the tumor environment.
Iron metabolism has been shown to play an important role in the development and function of the immune system, but its role in ILC3s is unclear. Here the authors show that CD71-mediated iron metabolism controls ILC3 proliferation and the host response to Citrobacterrodentium infection and CD71 expression is regulated by Ahr signaling.
Santosa et al. show that IRF4 is upregulated upon NK cell activation and acts as a signal integrator for the differentiation and expansion of mouse cytomegalovirus-specific NK cells by partly controlling nutrient uptake required for adaptive NK cell responses.
Chi and colleagues identify brain-resident CXCR6+PD-1+CD8+ T cells that interact with resident microglia to limit immune-mediated pathology in a mouse model of Alzheimer’s disease.
Here the authors show that TFPI2 promotes glioblastoma stem cell self-renewal and connects stemness to microglia immunosuppression, plus targeting TFPI2-mediated glioblastoma stem cell–microglia symbiosis inhibits tumor growth and synergizes with anti-PD1 therapy in glioblastoma.