Browse Articles

In this Review, Ho and colleagues focus on how myeloid cells detect and respond to oxygen availability in the local tissue microenvironment and discuss how acute and chronic hypoxia modulate myeloid cell functions.

Peanut oral immunotherapy reshapes T cell responses, suppressing allergy-associated type 2 helper T cells and boosting cytotoxic type 1 helper T cells, offering clues to long-term tolerance.

Huang and colleagues report that TIM4–AMPK signaling induces downregulation of the mitochondrial HSP90 chaperone TRAP1 in tumor-associated macrophages, thereby enhancing their immunoinhibitory function and promoting immune evasion and tumorigenesis.

Systemic hypoxia is sufficient to induce persistent neutrophil dysfunction in humans, months after acute respiratory distress syndrome or high-altitude conditions. This dysfunction is mediated by loss of the histone modification H3K4me3. In hypoxic mouse models, we show that this reduction in H3K4me3 originates in neutrophil progenitor populations and is a consequence of histone 3 clipping.

Walmsley and colleagues report that systemic hypoxia induces persistent loss of histone H3K4me3 marks and epigenetic reprogramming in neutrophil progenitors, resulting in long-term impairment of subsequent neutrophil effector functions.

Kallies and colleagues examine the role of the chromatin regulator SATB1 in CD8⁺ T cell differentiation during viral infection and cancer. They show that SATB1 is a negative regulator of exhausted CD8⁺ T cell expansion and effector differentiation.

TIGIT, a coinhibitory receptor that suppresses excessive immune responses, also promotes tissue regeneration by functioning as a co-stimulatory receptor in regulatory T cells via the TIGIT–TCR–BLIMP1–AREG axis during viral infection.

Research identifies MEF2C as a human-specific switch that keeps microglia in balance. Loss of MEF2C tips microglia toward inflammatory and aging-like states that link to autism and Alzheimer’s disease.

Coufal and colleagues generated microglia from human iPS cells to examine mechanistic roles of the transcription factor MEF2C and how these roles might relate to the autism phenotype seen following the loss of MEF2C in human microglia.

Grimes and colleagues integrate multiomic features to create a framework that allows the isolation of discrete cell states across hematopoiesis and exploit the underlying gene regulatory networks to identify lineage restriction within multilineage progenitors.

Single-cell transcriptomic analysis of blood CD4⁺ T cells from children with systemic lupus erythematosus (SLE) reveals an unexpected diversity of helper and regulatory cells that could underlie disease flares and organ damage.

Caielli and colleagues performed single-cell RNA sequencing on blood CD4⁺ T cells from pediatric patients with systemic lupus erythematosus and healthy donors, identifying naive, memory, T_reg, proliferative and interferon-stimulated gene-high cell subsets. Follicular and peripheral helper T cells, including T_H10 cells, and cytotoxic memory cell populations were expanded, along with dysfunctional T_reg cells marked by aberrant TLR5 and FCRL3 expression, pointing to links between microbial dysbiosis and impaired immune regulation.

Because they are a main source of the antiviral cytokines type I and III interferons, plasmacytoid dendritic cells are considered to be essential for host defense against viral infections. Contrary to this dogma, we show that they are dispensable or even detrimental in mice.

Brown and colleagues review the heterogeneity of mucosal antigen-presenting cells that orchestrate T cell immunity to intestinal antigens.

In this Review, the authors cover the immunology of cancer vaccines and how they can be used to boost the efficacy of immunotherapies for cancer.

A recent Nature paper presents findings that highlight brain fibroblasts as dynamic regulators of tissue repair and immunomodulation after injury, with implications for understanding scar formation, function and long-term outcomes of acute brain injuries.