Volume 26 Issue 11, November 2025

Innate lymphoid cells in the female genital tract have been understudied. A study now characterizes these cells, including their potential responses to HIV infection.

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.

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.

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.

The thymus produces T cells, and an improved understanding of thymus biology is likely to have therapeutic potential. Here we summarize the 2025 ThymUS conference, focusing on fundamental insights and translational potential.

Rapidly progressive glomerulonephritis refers to a group of severe autoimmune kidney diseases. Using high-resolution spatial transcriptomics, we identified a common pathway of disease progression and uncovered sequential PDGF and TGFβ activation of parietal epithelial cells as critical drivers of glomerulonephritis. Our study provides valuable insights that could result in disease stage-specific treatment options.

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.

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.

In this Review article, Vince et al. focus on recent developments in necroptotic cell death in health and disease.

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.

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

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.

Here the authors show how the DNA-sensing cGAS–STING pathway activates NF-κB and inflammatory gene expression with delayed kinetics via post-Golgi endolysosomal signaling.

DNA damage from chemotherapy can activate cGAS–STING and interferon pathways. Here, the authors show that cGAS–STING signaling is specific to DNA rich in CA repeats, whereas DNA not rich in CA repeats is detected by AIM2, resulting in opposing tumor immune responses.

Pucella, Maqueda-Alfaro and colleagues distinguish three developmentally related subsets of mouse plasmacytoid dendritic cells that differ in their ability to produce type I interferon and their susceptibility to virus.

Previous research has suggested that pDCs are required for an effective antiviral immune response, but direct experimental evidence to support this is lacking. Here Ngo et al. develop a pDC knockin mouse model and find that pDCs are dispensable for an antiviral immune response to mouse cytomegalovirus and may be detrimental during influenza or SARS-CoV-2 infection.

Here the authors provide a deep tissue analysis of patients with autoimmune kidney diseases, identifying a conserved spatiotemporal immune program for the development of glomerular crescents and sclerosis.

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.

Here the authors map the dynamics of human NK cell residency and recirculation, showing that CD56^bright NK cells transiently occupy tissues and recirculate via lymphatics, whereas CD56^dim NK cells remain vascular except during inflammation.

Klein and colleagues characterize 04_A06, a new V_H1-2-encoded broadly neutralizing antibody that has marked breadth and potency against extended multiclade HIV-1 pseudovirus panels and can maintain full viral suppression in HIV-1-infected humanized mice.

The authors spatially and functionally map innate lymphoid cells in the human female genital tract at homeostasis, uncovering tissue-specific and subset-specific distribution and functions, and rapid antiviral responses following HIV exposure.

The authors report that an AS03-adjuvanted chimeric hemagglutinin-based influenza vaccine induces persistent stalk-specific serum antibody and bone marrow plasma cell responses in nonhuman primates, offering promise for broader and durable flu protection.

Rudensky and colleagues demonstrate a context-dependent differential requirement for Foxp3 for T_reg cell transcriptional and functional programs.

Joller and colleagues show that the co-inhibitory receptor TIGIT induces the expression of the tissue growth factor amphiregulin (Areg) in regulatory T cells and contributes to tissue repair in response to viral infection.

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.

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.