bims-nimamd Biomed News
on Neuroimmunity and neuroinflammation in ageing and metabolic disease
Issue of 2026–08–02
twenty-two papers selected by
Fawaz Alzaïd, Sorbonne Université



  1. Nature. 2026 Jul 29.
      
    Keywords:  Animal behaviour; Neuroscience
    DOI:  https://doi.org/10.1038/d41586-026-02325-7
  2. Sci Immunol. 2026 Jul 31. 11(121): eaeg8653
      Peritoneal cavity fluid and mesothelial surfaces host distinct resident macrophage populations, among which include the well-described Gata6+ large cavity macrophages (LCMs) in peritoneal fluid. Here, we reveal that LCMs arise from two separable differentiation pathways. In the quantitatively minor pathway, monocytes gave rise to LYVE1+ LCMs but few Gata6+ LCMs. This pathway did not require the transcription factor Gata6 but was severely impaired in mice bearing three mutations in the -165 kb Zeb2 enhancer (Zeb2TM) with impaired monocyte development. The second, dominant pathway supported Gata6-dependent LCMs and was intact in Zeb2TM mice, even when turnover was enforced by irradiation, and was supported by adoptive transfer of a specialized LCM intermediate expressing Gata6 before the residency marker TIMD4. Functionally, the quantitatively minor LCM pathway distinctly surveilled the mesothelium, replenishing mesothelial border macrophages upon encountering an open niche. Thus, beyond embryonic versus adult hematopoietic paradigms, LCMs with overlapping and distinct phenotypes arise from two pathways linked to divergent fates.
    DOI:  https://doi.org/10.1126/sciimmunol.aeg8653
  3. Science. 2026 Jul 30. 393(6810): 467
      
    DOI:  https://doi.org/10.1126/science.aek0526
  4. Science. 2026 Jul 30. 393(6810): 461
      Changes in lysosomal metabolites are associated with both aging organs and lysosomal storage diseases.
    DOI:  https://doi.org/10.1126/science.aej5901
  5. Nat Commun. 2026 Jul 30. pii: 7598. [Epub ahead of print]17(1):
      Transposable elements are hypothesized to have driven gene regulatory innovation, yet their contributions to primate brain development at the cell type level remain underexplored. Here, we use single-cell multiomics data from human, macaque, marmoset, and mouse cerebella to show that transposable element contributions to different cell types are shaped by varying degrees of constraints across cell types, as well as the preferential co-option of certain transposable elements in specific cell states. Using a sequence-based deep-learning model that predicts cell-type-specific chromatin accessibility, we systematically assess the co-option potential of transposable elements into cerebellar gene regulatory networks, identifying twelve transposable element subfamilies with complex regulatory sequences in their ancestral states that facilitate their co-option as cell-type-specific cis-regulatory elements. Preservation of these ancestral regulatory sequences, as well as the active chromatin environment surrounding the insertion site, is the major determinant of the accessibility of extant copies. Lineage-specific accessible copies contribute to human-specific gene expression. Broadly, we demonstrate how transposable elements can be flexibly co-opted into cell-type-specific gene regulatory networks, and introduce a generalizable analytical framework for dissecting their contribution to mammalian regulatory evolution.
    DOI:  https://doi.org/10.1038/s41467-026-75700-7
  6. Nature. 2026 Jul 27.
      
    Keywords:  Brain; Molecular biology; Neuroscience
    DOI:  https://doi.org/10.1038/d41586-026-02294-x
  7. Science. 2026 Jul 30. 393(6810): eadz8081
      X-chromosome inactivation (XCI) enables gene dosage compensation in XX eutherians. Long interspersed element-1 (LINE-1 or L1) retrotransposons are unusually abundant on the human X chromosome and are hypothesized to facilitate XCI. Here, we used long-read DNA sequencing to conduct a haplotype-aware analysis of engineered L1 integration preferences in the PA-1 human embryonic carcinoma cell line. Crucially, clonal XCI in PA-1 cells enabled derivation of active (Xa) and inactive (Xi) X-chromosome haplotypes. L1 integration strongly favored the Xi and other genomic regions that undergo DNA replication late in S-phase. These results suggest that the X chromosome is L1 rich because of XCI and imply that L1 integration preference for the Xi in XX individuals could potentially double the frequency of X-linked pathogenic L1 mutations in their XY descendants.
    DOI:  https://doi.org/10.1126/science.adz8081
  8. Nature. 2026 Jul 29.
      Senescent cells promote tissue dysfunction in part through the senescence-associated secretory phenotype (SASP)1. Cytosolic mitochondrial nucleic acids activate innate immune signalling to initiate this inflammatory programme2,3. Here we show that mitochondrial metabolism provides a second layer of control that enables execution of the inflammatory programme. In senescent cells, the mitochondrial pyruvate-citrate-acetyl-CoA axis is upregulated, increasing the availability of acetyl-CoA to support histone acetylation at SASP genes. Whereas mitochondrial DNA-driven signalling activates inflammatory transcription factors, acetyl-CoA availability is required for robust transcription of SASP genes. Accordingly, enhancing acetyl-CoA levels promotes SASP gene expression, whereas inhibition of SLC25A1, the mitochondrial citrate exporter, reduces histone acetylation at SASP loci, limiting activity of this programme. In vivo, inhibition of SLC25A1 reduces chromatin accessibility at SASP loci, dampens inflammation and improves healthspan in aged mice. Together, these findings identify a mitochondrial metabolic checkpoint that enables the epigenetic execution of innate immune signalling, revealing a mechanism that selectively controls the inflammatory output of senescent cells.
    DOI:  https://doi.org/10.1038/s41586-026-10791-2
  9. Nat Commun. 2026 Jul 29. pii: 7588. [Epub ahead of print]17(1):
      When immune cells interact, they frequently exchange membrane-bound antigens. Our evolving understanding of these processes challenges the cellular specificity of lineage markers and therapeutic monoclonal antibodies. By using mouse and human B-T cell co-cultures, we report that CD19, an assumingly exclusive B cell marker, is transferred via trogocytosis when B cells activate T cells. In a B cell-driven model of experimental autoimmune encephalomyelitis, CD19+ T cells expand and show enhanced features of activation, differentiation, and encephalitogenic potential ex vivo. Additionally, co-transfer of CD19 and functional IgM from B cells results in the gain of B cell function by T cells. In patients with chronic central nervous system (CNS) demyelination, CD19+ T cells display a pro-inflammatory phenotype and are concomitantly depleted by inebilizumab, an approved anti-CD19 antibody, which raises important considerations for the therapeutic use of monoclonal antibodies overall. Finally, we report that myeloid cells acquire CD19 and functional IgM after phagocytosis of apoptotic B cells and thereby gain functional B cell properties. These findings highlight the commonness of membrane and antigen-transfer between cells, resulting in transmission of cellular function.
    DOI:  https://doi.org/10.1038/s41467-026-75534-3
  10. Immunity. 2026 Jul 30. pii: S1074-7613(26)00304-3. [Epub ahead of print]
      The liver-secreted protein fibrinogen-like protein 1 (FGL1) is a ligand of the coinhibitory receptor LAG3 on T cells; however, Fgl1-/- mice exhibit autoimmune features distinct from those of Lag3-/- mice. Here, we examined whether FGL1 acts via receptors beyond LAG3 to regulate autoimmunity. Recombinant FGL1 administration reduced autoimmune symptoms in B6/lpr lupus-like mice. This was associated with diminished antigen-specific IgM responses and B cell numbers. Genome-wide surface proteome screening identified the tumor necrosis factor receptor (TNFR) family member transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), a receptor for B cell-activating receptors BAFF and APRIL, as a receptor for FGL1. TACI bound FGL1 via an N-terminal site not required for BAFF and APRIL interaction. The impact of FGL1 administration on B cell numbers and autoimmune phenotypes was lost in Taci-/- mice. Mechanistically, FGL1 promotes TACI internalization, thereby regulating receptor availability for activating ligands. Thus, FGL1 regulates an innate-like subset of B cells via modulating TACI availability, with implications for autoimmunity and inflammation.
    Keywords:  APRIL; B cell; BAFF; BCMA; FGL1; LAG-3; TACI; autoimmunity; inhibitory; lupus
    DOI:  https://doi.org/10.1016/j.immuni.2026.07.005
  11. Nat Chem Biol. 2026 Aug;22(8): 1286-1298
      Identifying synergies between dietary fibers and beneficial bacteria holds promise for precision interventions that optimize gut health, yet these interactions remain largely unexplored. Here we integrate machine learning, Bayesian optimization and high-throughput community construction to investigate how dietary fibers shape health-relevant functions of human gut microbial communities. To efficiently navigate the landscape of fiber-microbiome interactions, we implemented a design-test-learn cycle to identify fiber-species combinations that maximize a multiobjective function capturing beneficial community properties. Our model-guided approach revealed a highly butyrogenic and robust ecological motif characterized by the copresence of inulin, Bacteroides uniformis and Anaerostipes caccae and a higher-order interaction with Prevotella copri. Human fecal communities invaded with model-designed species-fiber combinations displayed predictable gut-beneficial outputs. In sum, we demonstrate a framework for designing synthetic microbial communities with desired functions in response to key nutrients.
    DOI:  https://doi.org/10.1038/s41589-026-02272-4
  12. Nat Microbiol. 2026 Aug;11(8): 2349-2364
      The gut microbiota influences host metabolism, but the mechanisms of lipid uptake from food remain mysterious. Here we used stable isotope-labelled tracers in gnotobiotic mouse models, which revealed that host uptake of dietary lipids depends on microbial colonization. Systemic lipid metabolism modelling predicted that the gut microbiota restricts intestinal lipid absorption, and labelled lipid administration verified that the gut contents of microbiota-colonized mice contained up to 12-fold more lipids than those of germ-free animals. A combination of lipidomics and proteomics showed that gut microbes trigger Myd88 signalling, leading to a downregulation of hepatic Cyp7b1 activity and increased taurocholate production. Taurocholate stimulates phospholipase A1 activity in bile, causing the degradation of phosphatidylcholine that is essential for luminal micelle formation and lipid uptake. A diverse microbiome was associated with lower phosphatidylcholine content. This previously unrecognized host-gut microbiota interplay via enzymes in bile could provide future targets to modulate dietary lipid absorption.
    DOI:  https://doi.org/10.1038/s41564-026-02434-z
  13. Sci Signal. 2026 Jul 28. 19(948): eaek8307
      Chronic stress in mice causes anxiety and hyperglycemia by inducing senescence in amygdala astrocytes.
    DOI:  https://doi.org/10.1126/scisignal.aek8307