bims-traimu Biomed News
on Trained immunity
Issue of 2026–06–21
fifteen papers selected by
Yantong Wan, Southern Medical University
  1. Metabolic support of trained immune responses in myeloid cells.
  2. Human macrophages encode stimulus-specific information of prior exposures through trained immunity.
  3. HIV-1 Nef generates lasting innate immune memory in haematopoietic stem and progenitor cells in vivo.
  4. Effects of probiotic fermentation on Gracilaria bailinae polysaccharides: Characterization and immunomodulatory potency.
  5. Epigenetic Gene Networks Governing Immune State Transitions Across the Lifespan.
  6. Immunological effects of β-glucan as a trained immunity-based adjuvant in vaccinated goats against anthrax.
  7. Programming the immunological properties of mRNA vaccines for cancer.
  8. Interleukin-1-mediated inflammatory memory: Protective training or maladaptive tumor imprinting?
  9. Whole β-glucan particles modulate BCG-induced macrophage and CD4+ T-cell responses via the Dectin-1-JAK1/STAT1 pathway.
  10. p120-catenin enhances macrophage efferocytosis and facilitates resolution of lung inflammatory injury.
  11. β-1,3-Glucan mediates innate immunity and anti-aging effects in aged male Nothobranchius guentheri and protects against Aeromonas hydrophila infection.
  12. Bacterial infection reshapes monocyte and macrophage ontogeny at the CNS borders.
  13. A brain-lung circuit drives LPS-induced lung injury via sympathetic neutrophil axis.
  14. Remodeling of the immune-metabolic landscape triggered by long-term high-altitude exposure.
  15. Is the impact of malaria infection on immune memory of a clinical concern?
  1. Elife. 2026 Jun 19. pii: e108814. [Epub ahead of print]15
    Metabolic support of trained immune responses in myeloid cells.
    Aitor Jarit-Cabanillas, Gillian Dunphy, Federico Virga, Jan Van den Bossche, David Sancho.
      Trained immunity (TI) is defined as a form of innate immune memory characterised by a long-lasting ability to develop enhanced responses to a secondary challenge, whether of the same or a different nature than the initial stimulus. This process is mediated by several established hallmarks, most prominently the existence of activating epigenetic marks and metabolic adaptations. The activating epigenetic marks prime the expression of immune-related genes and are a direct driving force behind the increased cytokine production after secondary stimulation of trained monocytes and macrophages. Training stimuli also induce specific metabolic adaptations, such as the upregulation of glycolysis and lactate production or the activation of glutaminolysis leading to fumarate accumulation, which in turn promotes epigenetic changes. However, the mechanisms linking these epigenetic and metabolic changes to a TI phenotype are varied, and not all stimuli that increase glycolysis promote training, whereas some stimuli such as lipopolysaccharide (LPS) display a non-monotonic induction of TI. In addition to metabolism directly driving epigenetic changes, early gene expression changes can also reshape cell metabolism to promote a trained phenotype. In this review we aim to separate two main types of metabolic rewiring that have not been previously uncoupled. Firstly, those primary metabolic changes occurring during the initial stimulation, which precede TI induction by altering the epigenomic landscape around inflammatory genes. Secondly, those metabolic adaptations arising later as a consequence of the first wave of epigenetic regulation, which support an enhanced functional state of macrophages.
    Keywords:  immunology; inflammation; metabolism; myeloid cells; trained immunity
    DOI:  https://doi.org/10.7554/eLife.108814
  2. Cell Syst. 2026 Jun 19. pii: S2405-4712(26)00129-8. [Epub ahead of print] 101647
    Human macrophages encode stimulus-specific information of prior exposures through trained immunity.
    Aoife O'Farrell, Zijian Niu, Jingxin Li, Laura C Van Eyndhoven, Kavitha Sarma, Arjun Raj.
      Trained immunity (a form of innate immune memory) is defined in part by heightened responses to pathogen restimulation and can be generated by many different stimuli. However, both the quantitative differences in trained states generated by different stimuli and the downstream consequences of those differences remain unclear. Here, we used primary human monocyte-derived macrophages to demonstrate phenotypic and molecular stimulus specificity of trained immunity 6 days after initial exposure. Quantification of cytokine production with single-molecule RNA imaging revealed stimulus-specific patterns of response to restimulation, with trained cells showing stronger responses to secondary stimuli more similar to their initial stimulation. Differential licensing of inflammatory transcription factors was associated with encoding of specificities in chromatin 6 days after training, while memory of some, but not all, training stimuli was lost by 11 days post-training in vitro. Overall, our findings demonstrate that different training stimuli can impart specific memories that generate distinct training phenotypes.
    Keywords:  cellular learning; cellular memory; epigenetics; innate immune memory; innate immunity; macrophages; single-cell analysis; systems biology; trained immunity
    DOI:  https://doi.org/10.1016/j.cels.2026.101647
  3. EMBO Rep. 2026 Jun 15.
    HIV-1 Nef generates lasting innate immune memory in haematopoietic stem and progenitor cells in vivo.
    Andrew J Fleetwood, Nigora Mukhamedova, Dragana Dragoljevic, Man K S Lee, Yangsong Xu, Malathi S I Dona, Ian Hsu, Camilla Bertuzzo Veiga, Fumihiko Takeuchi, Ben Crossett, Denise Tran, Alexander R Pinto, Michael Bukrinsky, Andrew J Murphy, Dmitri Sviridov.
      HIV infection is accompanied by chronic inflammation-related co-morbidities, even when viral replication is suppressed by therapy. This persistent inflammatory state suggests that long-lived immune cell lineages may acquire stable pro-inflammatory programming. Here, we investigate whether inflammatory programming can be imprinted within hematopoietic lineages, following the exposure of mice and bone marrow-derived macrophages (BMDMs) to extracellular vesicles (EVs) carrying Nef, a key inflammatory factor of HIV. Multi-omics profiling shows that hematopoietic cells exposed to Nef-EVs undergo epigenetic remodeling and reprogramming of energy and lipid metabolism characteristic of trained innate immunity. The inflammatory phenotype in BMDMs is partially reversed by inhibition of glycolysis, a key metabolic driver of trained immunity. We demonstrate that following competitive bone marrow transplantation, hematopoiesis in mice receiving bone marrow from Nef-EV-treated donors displays a sustained bias toward myelopoiesis, and BMDMs retain enhanced inflammatory potential. These findings demonstrate that Nef-EVs can imprint a lasting inflammatory memory, mechanistically similar to trained immunity, in hematopoietic cells. This memory persists beyond the initial exposure and may contribute to chronic inflammation in people with HIV.
    DOI:  https://doi.org/10.1038/s44319-026-00838-w
  4. Int J Biol Macromol. 2026 Jun 17. pii: S0141-8130(26)03002-3. [Epub ahead of print] 153075
    Effects of probiotic fermentation on Gracilaria bailinae polysaccharides: Characterization and immunomodulatory potency.
    Suwen Hu, Qianmin Lin, Jieting Yu, Youhong Li, Wenshen Lin, Chun Yang, Hailang Cui, Riming Huang, Huaming Tao.
      Gracilaria bailinae polysaccharides have limited applications due to their high viscosity, large molecular weight, and poor solubility. Probiotic fermentation emerges as an efficient strategy to enhance the bioactivity of plant polysaccharides. This study aimed to prepare fermented water-soluble crude polysaccharide (GBV) from G. bailinae via fermentation with Bacillus velezensis, using water-extracted polysaccharide (GBP) as a control. The physicochemical properties, immunomodulatory activity, and trained immunity effects of GBV were systematically investigated. A significant decrease in molecular weight, accompanied by increased sulfate and uronic acid content, was observed in G. bailinae polysaccharides following fermentation. Modifications to the monosaccharide composition ratio and microstructure also occurred, though the basic polysaccharide structure remained unaffected. In vitro experiments revealed that both GBV and GBP were non-toxic to RAW264.7 macrophages and promoted cell proliferation, phagocytosis, and the secretion of nitric oxide (NO) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). Notably, GBV exhibited superior immunostimulatory activity at low concentrations (6.25-50 μg/mL) compared to GBP. Furthermore, at a concentration of 12.5 μg/mL, GBV was found to trigger trained immunity in RAW264.7 cells, as demonstrated by elevated levels of cytokines and NO following LPS restimulation. Untargeted metabolomics analysis indicated that the trained immunity effect was associated with metabolic reprogramming of purine, pyrimidine, and arginine-polyamine pathways, with significant downregulation of spermine potentially amplifying the M1 inflammatory phenotype. These findings demonstrate that B. velezensis fermentation improves the immunomodulatory activity of G. bailinae polysaccharides, and GBV holds great potential as a natural immune activator. These findings provide a theoretical foundation for the development and application of probiotic-fermented seaweed polysaccharides.
    Keywords:  Gracilaria bailinae; Macrophages; Metabolic reprogramming; Microbial fermentation; Polysaccharides; Trained immunity
    DOI:  https://doi.org/10.1016/j.ijbiomac.2026.153075
  5. Immunology. 2026 Jun 19.
    Epigenetic Gene Networks Governing Immune State Transitions Across the Lifespan.
    Ola A Al-Ewaidat, Moawiah M Naffaa.
      Immune function across development, tissue repair, aging, and disease depends not only on signaling pathways but also on epigenetic architectures that determine whether coordinated transcriptional programs can be accessed and resolved. Increasing evidence indicates that epigenetic gene networks regulate the accessibility and reversibility of semi-stable immune states, shaping plastic, homeostatic, reparative, and degenerative configurations. We propose the concept of epigenetic transition windows, defined as temporally and contextually restricted intervals during which epigenetic constraints are relaxed, permitting coordinated and reversible transitions between immune states. During development, these windows are broad and support immune tolerance and adaptive plasticity. In adulthood they become spatially and temporally restricted, preserving stability while enabling conditional adaptation. With aging, they progressively narrow, contributing to chronic inflammation, impaired repair, and increased vulnerability to neurodegeneration. Conversely, pathological persistence of regulatory permissiveness may underlie immune evasion and sustained plasticity in cancer. We outline operational genomic readouts for quantifying transition windows, including chromatin accessibility variance, enhancer switching dynamics, reversibility metrics, and cross-cell coordination indices, and derive experimentally testable predictions that distinguish this model from pathway-centric or damage-centric explanations. By reframing immune dysfunction as a failure of regulated state transition rather than excessive signaling alone, this framework integrates inflammaging, trained immunity, immune resolution failure, and tumor immune escape within a unified regulatory architecture and provides a systems-level perspective on immune adaptability across the lifespan.
    Keywords:  chromatin accessibility; epigenetic regulation; immune plasticity; immune resolution; immune state transitions; immunosenescence; inflammaging; trained immunity; tumor immune evasion
    DOI:  https://doi.org/10.1111/imm.70161
  6. Vet J. 2026 Jun 18. pii: S1090-0233(26)00204-2. [Epub ahead of print]318 106748
    Immunological effects of β-glucan as a trained immunity-based adjuvant in vaccinated goats against anthrax.
    Miriam Angulo, Carlos Angulo.
      Trained immunity-based adjuvants (TIbAs) have emerged as a promising strategy to enhance vaccine-induced protection through functional reprogramming of innate immune cells. The present study evaluated the adjuvant potential of β-glucan derived from Debaryomyces hansenii CBS8339 in a vaccine against anthrax in goats. Peripheral blood monocyte-like cells from vaccinated goats were assessed for effector and metabolic responses following ex vivo lipopolysaccharide stimulation. Co-administration of β-glucan and anthrax vaccine significantly enhanced crucial innate immune effector mechanisms, including phagocytic activity, nitric oxide production, and myeloperoxidase activity compared with control animals. Additionally, adjuvanted vaccination was associated with metabolic changes consistent with increased glycolytic activity (glucose consumption and lactate production). These findings suggest that β-glucan may function as a TIbA by enhancing innate immune responsiveness. Further studies are needed to elucidate the underlying molecular mechanisms and to determine the long-term implications of trained immunity-mediated adjuvanticity for improving vaccine performance.
    Keywords:  Inmunometabolic response; Innate immune memory; Livestock immunology; Vaccine adjuvantation
    DOI:  https://doi.org/10.1016/j.tvjl.2026.106748
  7. Nat Rev Immunol. 2026 Jun 19.
    Programming the immunological properties of mRNA vaccines for cancer.
    Annette Wu, Seong Dong Jeong, Benjamin R Schrank, Betty Y S Kim, Padmanee Sharma, Wen Jiang.
      Messenger RNA (mRNA) vaccines are a transformative platform for inducing antigen-specific T cell and B cell responses that are now being trialled in oncology. Here we propose an immunological framework that reconciles four axes controlling the efficacy of mRNA cancer vaccines: adjuvanticity versus immunopathology, antigen immunogenicity versus tolerance, adaptive immune memory versus exhaustion, and beneficial versus maladaptive trained immunity. We argue that mRNA vaccines should be viewed as programmable constructs in which nucleoside chemistry, delivery platforms and dosing schedules can be manipulated to tune these four axes by modulating antigen identity and decay, costimulation, cytokine tone and innate stimulation. By fitting recent mechanistic and translational insights into this framework, we outline design principles for positioning mRNA cancer vaccines within an optimal window of immune activation that supports durable, tumour-specific immunity while minimizing T cell exhaustion, tolerance and systemic toxicity.
    DOI:  https://doi.org/10.1038/s41577-026-01316-z
  8. Semin Immunol. 2026 Jun 15. pii: S1044-5323(26)00034-5. [Epub ahead of print]83 102047
    Interleukin-1-mediated inflammatory memory: Protective training or maladaptive tumor imprinting?
    Despoina Xanthopoulou, Maria Crespo, Lydia Kalafati.
      Interleukin-1 (IL-1) exerts a pivotal role in the regulation of innate immune responses and inflammatory processes. Beyond its local effects at the site of inflammation, IL-1 acts as a systemic regulator of hematopoiesis by reprogramming hematopoietic stem and progenitor cells (HSPCs), thereby shaping the functional properties of the myeloid progeny. Through induction of emergency myelopoiesis and inflammatory memory, IL-1 can imprint durable epigenetic, metabolic and transcriptomic changes within the hematopoietic compartment, altering immune output well beyond the initial inflammatory trigger. This systemic effect of IL-1 signaling is particularly relevant in the context of cancer, since tumors are now viewed as inflammatory entities providing persistent inflammatory factors that can influence hematopoiesis and imprint an immunosuppressive phenotype in myeloid cells. In parallel, aging and clonal hematopoiesis (CH) are characterized by chronic low-grade inflammation in which IL-1 signaling may amplify mutant progenitor expansion, linking inflammaging to increased susceptibility to both hematological malignancies and solid cancers. Here, we discuss the role of IL-1 signaling in emergency myelopoiesis and both central and peripheral inflammatory memory, and how these processes shape cancer progression. We also highlight the therapeutic potential of targeting IL-1-mediated hematopoietic reprogramming.
    Keywords:  Cancer progression; Emergency myelopoiesis; Hematopoietic reprogramming; IL-1 signaling; Inflammatory memory; Systemic inflammation
    DOI:  https://doi.org/10.1016/j.smim.2026.102047
  9. Commun Biol. 2026 Jun 17.
    Whole β-glucan particles modulate BCG-induced macrophage and CD4+ T-cell responses via the Dectin-1-JAK1/STAT1 pathway.
    Yige Cao, Haoran Qu, Qing Tian, Sujuan Sun, Wenwen Zhang, Dan Fang, Pinru Chen, Chenyu Zhao, Xiao-Lian Zhang, Qin Pan, Fengling Luo, Min Liu.
      Tuberculosis (TB) remains a major global health burden, and Bacille Calmette-Guérin (BCG) provides inconsistent protection against adult pulmonary disease. Adjuvant strategies to enhance BCG efficacy are urgently needed. Here we show that whole β-glucan particles (WGP) enhance BCG-induced immune responses and improve protection against mycobacterial challenge. In vitro, WGP enhances macrophage functions associated with antigen processing during BCG exposure, including phagocytosis, lysosomal acidification, intracellular degradation, and the upregulation of MHC-II/CD80/CD86. WGP co-exposure partially attenuates the early IL-10 response induced by BCG. Mechanistically, whole β-glucan particles activate the Dectin-1-JAK1-STAT1 pathway, and disruption of this axis reduces MHC-II upregulation and impairs macrophage-supported OT-II CD4+ T-cell proliferation and IFN-γ production. In vivo, using female wild-type and Dectin-1 knockout C57BL/6 J mice, we find that split-site administration of WGP and BCG is better tolerated than same-site mixing and is associated with a less inflammatory early pulmonary myeloid profile. Under this optimized regimen, WGP plus BCG enhances CD4+ memory-associated responses and improves bacterial control while reducing lung inflammation in a Mycobacterium tuberculosis H37Ra challenge model. These findings support further evaluation of WGP as an adjunct candidate for BCG-based vaccination strategies and may inform the development of improved tuberculosis vaccines.
    DOI:  https://doi.org/10.1038/s42003-026-10492-6
  10. J Immunol. 2026 Jun 07. pii: vkag109. [Epub ahead of print]215(6):
    p120-catenin enhances macrophage efferocytosis and facilitates resolution of lung inflammatory injury.
    Jianguo Wang, Paulraj Kanmani, Guochang Hu.
      Defective resolution of inflammation following sepsis contributes to persistent immune dysfunction and increased morbidity and mortality worldwide. Efficient clearance of apoptotic polymorphonuclear neutrophils (PMNs) by macrophages, a process known as efferocytosis, is essential for resolving inflammation, promoting tissue repair, and restoring immune homeostasis; however, the molecular mechanisms governing this process remain poorly understood. Here, we identify p120-catenin (p120) as a critical regulator of efferocytosis that promotes the resolution of inflammatory lung injury. In alveolar macrophage-depleted mice challenged with endotoxin, intratracheal instillation of p120-deficient macrophages delayed the resolution of PMN infiltration, protein exudation, and lung edema and injury compared with control macrophages. These changes were accompanied by increased levels of TNF-α and IL-6, decreased levels of TGF-β and IL-10, and a reduced number of macrophages containing apoptotic PMNs in bronchoalveolar lavage fluid. p120 depletion also markedly reduced the phagocytosis of apoptotic PMNs by cultured macrophages. Mechanistically, p120 deficiency decreased the expression of the efferocytic receptors CD36 and Axl and shifted macrophage polarization toward a pro-inflammatory M1 phenotype. Furthermore, apoptotic cells induced the association and co-localization of p120 with peroxisome proliferator-activated receptor-γ (PPARγ), whereas p120 deletion markedly reduced PPARγ activity in response to apoptotic PMNs. Pharmacologic inhibition of PPARγ abolished p120-mediated macrophage efferocytosis and the resolution of lung inflammation. Collectively, these findings establish a central role for p120 in macrophage efferocytosis and inflammatory resolution and suggest that targeting macrophage p120 may represent a novel therapeutic strategy to promote recovery from inflammatory lung injury.
    Keywords:  efferocytosis; inflammation; lung injury; macrophage; sepsis
    DOI:  https://doi.org/10.1093/jimmun/vkag109
  11. J Fish Biol. 2026 Jun 18.
    β-1,3-Glucan mediates innate immunity and anti-aging effects in aged male Nothobranchius guentheri and protects against Aeromonas hydrophila infection.
    Lili Song, Haixia Qiao, JinPing Lan, Kang An, Yong Huang.
      Immunosenescence, a hallmark of aging, increases susceptibility to microbial infections and chronic inflammation. Here, we explored age-related innate immune alterations and the anti-aging potential of β-1,3-glucan using the short-lived annual fish Nothobranchius guentheri. A comparison of 6-month-old (adult) and 9-month-old (aged) male fish revealed that aging downregulated key innate immune genes (bf, C3, lysozyme, mbl1, mbl2, nk-lysin, β-defensin) while upregulating pro-inflammatory cytokines (interferon-γ, tnf-α) in the spleen, head kidney and liver. Aged fish were also much more susceptible to Aeromonas hydrophila infection, pointing to the occurrence of immunosenescence and inflammaging. Given this deteriorated immune status in aged fish, we next investigated whether β-1,3-glucan could alleviate age-associated immune dysfunction and resist bacterial pathogen invasion. The data demonstrated that β-1,3-glucan pretreatment significantly improved the survival rate of aged fish (53.00% ± 3.33% vs. 33.00% ± 3.33% in controls) and reduced bacterial loads in immune tissues. Mechanistically, β-1,3-glucan enhanced infection-induced expression of complement, mannan-binding lectin pathway and antimicrobial peptide genes, while suppressing excessive pro-inflammatory cytokine production in a time-dependent (6-24 h post-infection) manner. Collectively, our results demonstrate that β-1,3-glucan mitigates immunosenescence in aged N. guentheri by balancing antimicrobial defence and inflammatory responses, highlighting its potential as a nutritional intervention for enhancing innate immunity and combating age-related infection susceptibility.
    Keywords:  Nothobranchius guentheri; immunosenescence; inflammaging; innate immune; β‐1,3‐glucan
    DOI:  https://doi.org/10.1111/jfb.70546
  12. Sci Immunol. 2026 Jun 19. 11(120): eaee9584
    Bacterial infection reshapes monocyte and macrophage ontogeny at the CNS borders.
    Vitka Gres, Florens Lohrmann, Vidmantė Fuchs, Jana Neuber, Zohreh Mansoori Moghadam, Anne K Lösslein, Lance F P Bosch, Tiago Figueiral-Martins, Sebastian Baasch, David Obwegs, Gianni Monaco, Julia Henschel, Klaus P Knobeloch, Marco Prinz, Steffen Jung, Katrin Kierdorf, Sagar, Julia Kolter, Daniel Erny, Philipp Henneke.
      Macrophages in the meninges contribute to immune defense of the central nervous system (CNS), yet their site-specific origin and function remain poorly understood. Using an intravenous model of streptococcal meningoencephalitis in mice, we found bacteria predominantly in the leptomeninges and dura. Nevertheless, monocyte infiltration into the leptomeninges and parenchyma strongly correlated with disease severity. In the dura, infection triggered activation and loss of resident macrophages, followed by rapid engraftment of inflammatory monocytes that transiently replenished the macrophage niche. Under homeostasis, dural monocytes were supplied CCR2 independently from adjacent skull bone marrow. During infection, this local source was insufficient, necessitating recruitment from peripheral bone marrow. Infection further reshaped monocyte ontogeny, increasing monocyte-dendritic cell progenitor-derived monocytes, which expressed higher major histocompatibility complex class II levels and persisted in the brain alongside CD4+ T cells during resolution. Together, these findings reveal dynamic, compartment-specific remodeling of monocyte recruitment and differentiation across CNS borders during bacterial meningoencephalitis.
    DOI:  https://doi.org/10.1126/sciimmunol.aee9584
  13. J Neuroinflammation. 2026 Jun 16.
    A brain-lung circuit drives LPS-induced lung injury via sympathetic neutrophil axis.
    Shichun Ren, Shuo Yang, Baotong Liu, Qian Zhang, Zhenzhen Zhao, Yan Meng, Qi Shao, Xiaoming Deng, Jinjun Bian, Li Cao, Fengfeng Mo, Jiafeng Wang.
      Acute respiratory distress syndrome (ARDS) is a fatal complication of sepsis. However, the neural mechanisms underlying the exacerbation of pulmonary inflammation during systemic infection remain largely undefined. We employed an intraperitoneal lipopolysaccharide (LPS)-induced systemic inflammatory lung injury model and found that systemic inflammation strongly activates corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN), whereas bilateral subdiaphragmatic vagotomy abolished this response. Chemogenetic inhibition of CRHPVN neurons alleviated lung injury and the formation of neutrophil extracellular traps (NETs), whereas chemogenetic activation of CRHPVN neurons exacerbated pathological damage through sympathetic efferent signaling. Additionally, in patients with septic ARDS, β2-adrenergic receptor (ADRB2) expression was upregulated on neutrophils, and ADRB2 signaling delayed neutrophil apoptosis through the PI3K/Akt pathway, whereas ADRB2 blockade promoted neutrophil apoptosis and attenuated lung injury. In summary, we delineate a dysregulated neuroimmune axis in LPS-induced lung injury: systemic inflammatory signals activate the vagal afferent-PVN-sympathetic circuit, which in turn drives a neutrophil-mediated ADRB2-PI3K/Akt signaling pathway that amplifies lung injury. Our study reveals a mechanistic basis for neuroregulatory intervention and indicates that targeting this Brain-lung pathway may offer new therapeutic strategies for ARDS.
    Keywords:  ALI; ARDS; Neutrophils; PI3K/Akt signaling pathway; Sepsis; Sympathetic nerve; β2-Adrenergic receptors
    DOI:  https://doi.org/10.1186/s12974-026-03914-z
  14. Cell Rep. 2026 Jun 18. pii: S2211-1247(26)00454-7. [Epub ahead of print]45(7): 117376
    Remodeling of the immune-metabolic landscape triggered by long-term high-altitude exposure.
    Jiaqi Wang, Yutong Dong, Ruoyi Xue, Yi Huang, Wubin Yang, Chen Zhang, Yangkai Zhang, Fengsheng Wang, Ran Yang, Jiangjun Wang, Meng Yu, Yixiao Xu, Manying Guo, Yanping Tian, Rui Jian, Junlei Zhang, Yan Ruan, Yan Hu.
      Immunometabolic remodeling drives adaptation to long-term high-altitude exposure (LTHAE), yet the underlying mechanisms remain elusive. By integrating single-cell transcriptomics and metabolomics from 46 lowlanders following a 90-day LTHAE, we identified a strategy of "innate activation and adaptive suppression." Neutrophils exhibited enhanced maturation and phagocytosis, whereas adaptive immunity was dampened, characterized by suppressed B cell function and T cell responsiveness. Metabolically, LTHAE induced systemic shifts in steroid and amino acid metabolism associated with immune remodeling. Furthermore, multi-omics integration indicated a conserved upregulation of the glycolysis-TCA-OXPHOS axis across immune lineages, a metabolic adaptation supported by enzymatic assays in hematopoietic tissues of a hypobaric hypoxia mouse model. Collectively, these findings provide integrated insights into immune-metabolic landscape remodeling and suggest a potential mutual regulatory relationship between immune and metabolic state following LTHAE, offering a molecular foundation for high-altitude adaptation research.
    Keywords:  CP: immunology; CP: metabolism; high-altitude exposure; hypoxia adaptation; immune dysregulation; metabolic reprogramming; single-cell transcriptomics
    DOI:  https://doi.org/10.1016/j.celrep.2026.117376
  15. Expert Rev Clin Immunol. 2026 Jun 14.
    Is the impact of malaria infection on immune memory of a clinical concern?
    Katsuyuki Yui, Maria Lourdes Macalinao, Julius Hafalla.
      
    Keywords:  IL-10; IL-27; T cells; cytokine; immune pathology; immune response; malaria; vaccine
    DOI:  https://doi.org/10.1080/1744666X.2026.2688976
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