The study, published in the journal 3 Biotech, was led by Dongmei Liu of Lianyungang TCM Hospital at Nanjing University of Chinese Medicine, together with colleagues including corresponding author Xiaoyong Xu of the Fourth Affiliated Hospital of Nanjing Medical University. Rather than recruiting new patients, the team mined publicly available peripheral-blood transcriptomic datasets, turning archived gene-expression measurements into a fresh window on the immune biology of sepsis. Their analysis converged on a signature centered on two molecules with well-established roles in immune suppression: the transcription factor STAT3 and the enzyme arginase 1, known as ARG1.

The researchers built their discovery around a dataset known as GSE28750, which contained whole-blood expression profiles from ten sepsis patients and twenty healthy controls. Differential expression analysis identified 482 genes whose activity distinguished septic blood from healthy blood, with 301 genes ramped up and 181 dialed down. The direction of these changes told a coherent story. Genes associated with myeloid cells, the family of innate immune cells that includes monocytes and neutrophils, were prominently upregulated, as were genes tied to immunoregulatory function. Meanwhile, two of the most important flags of immune competence, the HLA-DRA and HLA-DRB1 genes that help immune cells display fragments of pathogens to T cells, were significantly downregulated, a molecular echo of the impaired antigen presentation that characterizes septic immunoparalysis.

Enrichment analysis sharpened the picture. The upregulated genes clustered in pathways governing myeloid cell activation, IL6-JAK-STAT3 signaling, and arginine metabolism, while pathways responsible for antigen processing and presentation were depleted. Each of these threads converges on a cell type that has become a central character in sepsis research: the myeloid-derived suppressor cell, or MDSC. These immature myeloid cells, which expand dramatically during sepsis, dampen T-cell responses through a repertoire of mechanisms, including the depletion of arginine by arginase enzymes, starving lymphocytes of a nutrient they need to proliferate and function.

To quantify this shift, the team applied single-sample gene set enrichment analysis, or ssGSEA, a computational technique that estimates the activity of predefined gene signatures in bulk expression data. Sepsis samples scored markedly higher on an MDSC-like signature than healthy controls, with a mean score of 0.72 plus or minus 0.21 compared with minus 0.36 plus or minus 0.18 in controls, a difference that reached a P value of 1.1 times ten to the minus seven. In plain terms, the blood of septic patients did not merely show scattered signs of immune disturbance; it carried a coordinated, statistically robust imprint of suppressive myeloid remodeling.

The critical question for any biomarker study is whether the finding holds beyond the data in which it was discovered. The researchers therefore turned to an independent validation cohort, GSE65682, comprising 120 sepsis-related samples drawn at baseline or ICU admission alongside 40 healthy controls. There, they checked that the candidate genes moved in the same direction as in the discovery set and tested the performance of a composite signature built from the key genes. The composite score achieved an area under the receiver operating characteristic curve, or AUC, of 0.94 in the discovery cohort and 0.88 in the validation cohort, values that indicate strong discriminatory power for separating septic patients from healthy individuals, though the authors frame this as exploratory diagnostic performance rather than a clinically validated test.

The choice of STAT3 and ARG1 as the signature’s anchors is biologically telling. STAT3 is a signaling hub downstream of interleukin-6 and other inflammatory cytokines, and its persistent activation in myeloid cells is a recognized driver of suppressor-cell differentiation, promoting the expansion of cells that blunt adaptive immunity. ARG1, the gene encoding arginase 1, is one of the classic effector molecules of these cells, catabolizing arginine in the microenvironment and thereby constraining T-cell responses. Recent work cited by the authors has shown that blocking arginase activity in a specific neutrophil subset can combat sepsis-induced lymphopenia, the loss of lymphocytes that leaves survivors vulnerable to secondary infections. The new signature thus captures, in transcriptomic terms, a pathway whose perturbation is already being explored therapeutically.

The study arrives amid a broader effort to bring genomic precision to critical care. A consensus blood transcriptomic framework for sepsis published in Nature Medicine in 2025 and a companion consensus immune dysregulation framework reflect a growing recognition that sepsis is not a single disease but a spectrum of host responses that may demand different treatments. Monocyte HLA-DR expression, the cell-surface readout of the antigen-presentation machinery whose genes the new study found downregulated, has been monitored in septic shock cohorts for two decades and remains a focal point for trials of immunostimulatory agents such as GM-CSF. A compact gene signature measurable from bulk blood, requiring no flow cytometry or specialized cell sorting, could complement these approaches and fit more easily into routine laboratory workflows.

The authors are careful about the limits of their work. The analysis relied on bulk transcriptomics, which measures average gene activity across mixed cell populations and cannot resolve which specific cells express which genes; single-cell studies have, however, independently identified immunosuppressive HLA-DR-low monocyte populations in sepsis, lending plausibility to the bulk-level signal. The validation cohort confirmed directionality and composite performance but did not test whether the signature predicts mortality, tracks disease trajectory over time, or distinguishes sepsis from other causes of critical illness. And because the data come from public repositories, the findings await prospective evaluation in newly recruited, diverse patient populations before any diagnostic use could be contemplated.

Even so, the study offers something the sepsis field badly needs: a transparent, reproducible pipeline. The authors report that processed expression matrices, candidate-gene lists, the complete immune-signature gene sets, and the R analysis scripts are available from the corresponding author on reasonable request, and the underlying data are freely accessible through the Gene Expression Omnibus. In a discipline where irreproducible biomarker claims have slowed progress, that openness matters. If future studies confirm and extend the STAT3-ARG1-associated myeloid signature, clinicians may one day add a molecular gauge of immune suppression to the vital signs and lab panels that currently guide sepsis care, identifying which patients need not just antibiotics and fluids, but a deliberate effort to restart a silenced immune system.

Subject of Research: A bulk peripheral-blood transcriptomic signature associated with STAT3 and ARG1 reflecting myeloid immunosuppression in sepsis

Article Title: Bulk peripheral-blood transcriptomic analysis identifies a STAT3/ARG1-associated myeloid immunosuppressive signature in sepsis

Article References: Bulk peripheral-blood transcriptomic analysis identifies a STAT3/ARG1-associated myeloid immunosuppressive signature in sepsis. (n.d.). https://doi.org/10.1007/s13205-026-05087-1

Image Credits: AI Generated

DOI: 10.1007/s13205-026-05087-1

Keywords: sepsis, transcriptomics, STAT3, ARG1, myeloid-derived suppressor cells, immunosuppression, biomarker, gene expression, ssGSEA, HLA-DR, IL6-JAK-STAT3 signaling, diagnostics

The research team approached the question with a strategy that has become increasingly powerful in the era of publicly available genomic data: integrated bioinformatics combined with machine learning. Rather than recruiting new patients, the investigators mined transcriptomic datasets deposited in the Gene Expression Omnibus, a public repository maintained by the National Center for Biotechnology Information that archives gene expression profiles from thousands of studies. By pulling together datasets from patients with sepsis and datasets from patients with thoracic aortic aneurysm, the team could compare, on a genome-wide scale, which genes are switched on or off in each condition and, crucially, which changes appear in both.

The first analytical step was the identification of shared differentially expressed genes, abbreviated DEGs. Differentially expressed genes are those whose activity levels, measured as messenger RNA abundance, differ significantly between diseased and healthy tissue. When the researchers cross-referenced the gene lists derived from sepsis samples with those derived from aneurysm samples, they found 193 genes that were perturbed in both diseases. This number is small relative to the roughly 20,000 protein-coding genes in the human genome, which is precisely what makes it interesting: it represents a narrow molecular intersection where two clinically distinct pathologies converge.

To understand what these 193 shared genes actually do, the team performed functional enrichment analysis and gene set enrichment analysis, two complementary computational techniques that ask whether a group of genes is overrepresented in known biological pathways. The results pointed strongly toward the immune system. The shared genes were significantly enriched in pathways governing T cell activation, the process by which cytotoxic and helper T lymphocytes ramp up their defensive machinery, and in Th17 cell differentiation, the maturation of a pro-inflammatory T cell subset that has been implicated in autoimmunity and chronic inflammation. Alongside these immune pathways, the analysis flagged oxidative stress–related processes, the cellular damage that accrues when reactive oxygen species overwhelm antioxidant defenses.

This combination of findings is biologically coherent. Both sepsis and aneurysm formation involve inflammation of the vasculature and damage to the structural integrity of blood vessel walls. In sepsis, a cytokine storm can injure the endothelial lining of vessels throughout the body; in thoracic aortic aneurysm, chronic inflammation and oxidative stress degrade the elastic fibers and smooth muscle that keep the aortic wall strong. The new study suggests that these are not merely superficial parallels but reflect overlapping gene regulatory programs, with T cell–driven immunity and oxidative metabolic stress acting as common threads.

Identifying shared genes is only the beginning, however. A true diagnostic biomarker must do more than appear altered in disease; it must reliably distinguish patients from healthy individuals, and ideally it should do so across independent cohorts measured in different laboratories. To filter the 193 candidates down to the most promising markers, the researchers deployed sequential machine learning algorithms. Machine learning models can weigh the expression patterns of thousands of variables and identify the subset of features that carries the most discriminatory information, a task that is intractable by simple visual inspection of expression matrices.

Through this sequential screening process, five candidate genes emerged: ARG1, IL18R1, LIX1L, TRIM32, and PRKCH. Each has a plausible connection to the biology at play. ARG1 encodes arginase 1, an enzyme that metabolizes the amino acid arginine and participates in inflammatory and urea-cycle metabolism. IL18R1 is the receptor for interleukin-18, a potent pro-inflammatory cytokine involved in innate immunity. LIX1L, TRIM32, and PRKCH are less familiar names but are involved in cellular stress responses, protein regulation, and intracellular signaling respectively. When the team checked the expression patterns of these five genes across independent datasets, the patterns were generally reproducible, an important validation step in any biomarker study, since findings that hold only in a single cohort are frequently artifacts of batch effects or small sample sizes.

The researchers then asked whether the expression of these five genes tracked with the immune landscape of the diseased tissues. Using immune infiltration analysis, a computational method that estimates the proportions of different immune cell types present in a bulk tissue sample based on gene expression signatures, they found that the candidate genes’ expression levels were associated with the estimated abundance of immune cell populations. This supports the idea that the genes are not passive bystanders but are intertwined with the immune cell activity that characterizes both sepsis and aneurysm tissue.

To move from correlation toward mechanism, the team turned to an experimental model. They treated vascular smooth muscle cells, the contractile cells that form the bulk of the aortic wall’s muscular layer, with lipopolysaccharide, or LPS, a molecule derived from the outer membrane of Gram-negative bacteria that is a standard laboratory trigger of inflammatory responses. In these LPS-treated vascular smooth muscle cells, ARG1 and IL18R1 were upregulated, meaning their expression increased, while LIX1L was downregulated. This experiment is significant because vascular smooth muscle cells are central to aneurysm pathology, and showing that bacterial inflammatory stimulation shifts the expression of the candidate genes in these cells provides a direct experimental link between the infection-driven biology of sepsis and the vessel wall remodeling that underlies aneurysm formation.

The authors conclude that sepsis and thoracic aortic aneurysm share common transcriptional signatures involving immune dysregulation and metabolic stress, and that ARG1 and IL18R1 in particular may represent candidate molecular features associated with inflammatory and vascular responses in both diseases. The study is, by design, computational and exploratory: it relies on public datasets, estimated immune cell proportions, and a single cell-culture experiment, so the five-gene signature will need prospective clinical validation before it could inform diagnosis or risk stratification for either condition. Nevertheless, the work adds to a growing body of evidence that diseases long treated as unrelated can share deep molecular roots, and it offers a concrete, testable set of targets for future studies of how systemic inflammation reshapes the vasculature. If those targets hold up, the same molecular markers might one day help clinicians identify which patients with overwhelming infection are also silently accruing damage to their aortas, turning a chance molecular overlap into genuine clinical foresight.

Subject of Research: Shared diagnostic biomarkers and immune-related mechanisms between sepsis and thoracic aortic aneurysm

Article Title: Identification of shared diagnostic biomarkers and immune-related mechanisms between sepsis and thoracic aortic aneurysm based on integrated bioinformatics and machine learning approaches

Article References: She, C., Deng, H., Feng, Y., Long, C., & Wu, J. (2026). Identification of shared diagnostic biomarkers and immune-related mechanisms between sepsis and thoracic aortic aneurysm based on integrated bioinformatics and machine learning approaches. PLOS One, 21(10), e0359784. https://doi.org/10.1371/journal.pone.0359784

Image Credits: AI Generated

DOI: 10.1371/journal.pone.0359784

Keywords: sepsis, thoracic aortic aneurysm, biomarkers, machine learning, bioinformatics, immune infiltration, transcriptomics, ARG1, IL18R1, vascular smooth muscle cells, oxidative stress, T cell activation

The enzyme in question is lysine methyltransferase 9, or KMT9, a histone-modifying protein that previous work from the same group had already implicated in prostate tumor growth and androgen receptor signaling. In the new study, published in the journal Molecular Cancer, Jon Peñarando, Eric Metzger, Roland Schüle, and colleagues demonstrate that KMT9 does far more than drive cancer cell proliferation. It actively constructs the molecular barriers that prevent the immune system from recognizing and destroying the tumor, making it a uniquely attractive target for combination approaches designed to sensitize prostate cancer to immunotherapy.

At the center of the discovery is a chemokine signaling axis that functions as a cellular summons for immunosuppressive cells. The researchers found that KMT9 regulates the expression of C-X-C motif chemokine ligands, including CXCL5, which are secreted by prostate tumor cells and bind to the C-X-C motif chemokine receptor 2, CXCR2, on the surface of circulating myeloid cells. This ligand-receptor interaction acts as a homing beacon, drawing polymorphonuclear myeloid-derived suppressor cells, or PMN-MDSCs, into the tumor. Once recruited, these cells populate the tumor immune microenvironment in large numbers, creating a dense myeloid shield around the malignant glands.

PMN-MDSCs are among the most potent enemies of antitumor immunity. They suppress cytotoxic T cell responses through multiple mechanisms, including depletion of the amino acid arginine, production of reactive oxygen species, and interference with T cell trafficking. Using genetically engineered mouse models of prostate cancer in which Pten and Trp53, two frequently altered tumor suppressor genes, are deleted in prostate epithelium, the team showed that tumors with intact KMT9 were heavily infiltrated by these suppressive myeloid cells. When the researchers ablated the Kmt9a gene specifically in the prostate, the picture changed dramatically: PMN-MDSC recruitment collapsed, and cytotoxic T cells flooded into the tumor glands, showing clear signs of activation such as granzyme B expression.

The spatial dimension of this effect proved just as important as the cellular one. Advanced single-cell spatial phenotyping revealed that in tumors with functional KMT9, cytotoxic T cells were largely excluded from the tumor epithelium, lingering instead in the surrounding stroma where they could not make contact with their targets. This immune-excluded pattern is one of the recognized hallmarks of tumors that resist checkpoint blockade, since drugs like anti-PD-1 antibodies can only reinvigorate T cells that are physically close to the cancer cells they are meant to kill. Loss of KMT9 converted this excluded architecture into an inflamed, T cell-infiltrated landscape, precisely the configuration associated with immunotherapy responsiveness.

But KMT9’s contribution to immune evasion did not end with recruitment of suppressor cells. In a second, mechanistically distinct arm of the study, the researchers found that KMT9 also arms the tumor cells themselves against T cell attack. Chromatin immunoprecipitation sequencing showed that KMT9 binds directly to the promoter of the gene encoding arginase 1, ARG1, an enzyme that catabolizes L-arginine, an amino acid essential for T cell function and proliferation. By driving ARG1 expression in prostate tumor cells, KMT9 renders them resistant to T cell-mediated cytotoxicity, effectively allowing them to survive even when killer lymphocytes do manage to engage them.

The therapeutic implications of this dual mechanism were tested in preclinical experiments. When mice carrying Kmt9a-deficient prostate tumors were treated with SB225002, a CXCR2 inhibitor, tumor growth was inhibited to a greater degree than with either intervention alone, confirming that the chemokine axis is a clinically relevant vulnerability downstream of KMT9. Similarly, combining Kmt9a loss with numidargistat, a pharmacological inhibitor of ARG1, produced enhanced suppression of tumor growth. These combination experiments suggest that even partial disruption of the KMT9 pathway could be amplified by drugs that target the individual immune-evasion mechanisms it controls.

Importantly, the team connected their mouse findings to human disease by analyzing data from the TCGA prostate adenocarcinoma cohort, which comprises 500 prostate tumor samples and 52 healthy prostate controls. The analysis showed that KMT9 expression is elevated in prostate tumors relative to normal tissue and that high KMT9 levels correlate with shorter progression-free survival, underscoring the clinical relevance of the pathway. The consistency between the murine genetic models, the human genomic data, and the pharmacological studies lends considerable weight to the conclusion that KMT9 is not an artifact of a single experimental system but a genuine driver of immune evasion in prostate cancer.

For a field searching for ways to unlock immunotherapy in prostate cancer, the study offers a compelling conceptual framework. Rather than targeting the tumor’s defenses one at a time, inhibiting KMT9 would strike at the epigenetic master switch that controls both the recruitment of immunosuppressive myeloid cells through CXCR2 ligand expression and the intrinsic resistance of tumor cells through ARG1. Ablation of KMT9α in the mouse models produced inhibition of prostate tumor growth accompanied by a massive reduction in PMN-MDSC recruitment and a significant increase in cytotoxic T cell activation and infiltration of the tumor glands, a triple effect that few single agents have achieved in this disease.

Considerable work remains before these findings reach the clinic. KMT9 inhibitors are still in early stages of development, and the safety of systemically targeting a methyltransferase with functions in normal tissue is not yet established. The study’s authors note that their findings establish KMT9 as a therapeutic target to reprogram the immunosuppressive landscape and potentially improve the clinical efficacy of current immunotherapies, a formulation that anticipates future trials combining KMT9-directed agents with checkpoint blockade. If those efforts succeed, the stubborn resistance of prostate cancer to immunotherapy, one of the most frustrating puzzles in modern oncology, may finally begin to yield, not to a smarter antibody or a stronger checkpoint inhibitor, but to an epigenetic enzyme that had been quietly building the tumor’s defenses all along.

Subject of Research: The role of the lysine methyltransferase KMT9 in shaping the immunosuppressive tumor immune microenvironment of prostate cancer

Article Title: KMT9 drives T cell exclusion and dysfunction by promoting PMN-MDSCs infiltration and ARG1 expression in prostate cancer

Article References: Peñarando, J., Willmann, D., Sum, M., Jia, Y., Berlin, C., Braun, L. M., Chen, Z., Urban, S., Jung, M., Duteil, D., Metzger, D., Gratzke, C., Zeiser, R., Greschik, H., Schüle, R., & Metzger, E. (2026). KMT9 drives T cell exclusion and dysfunction by promoting PMN-MDSCs infiltration and ARG1 expression in prostate cancer. Molecular Cancer. https://doi.org/10.1186/s12943-026-02801-8

Image Credits: AI Generated

DOI: 10.1186/s12943-026-02801-8

Keywords: KMT9, prostate cancer, tumor immune microenvironment, PMN-MDSCs, CXCL5, CXCR2, ARG1, cytotoxic T cells, cancer immunotherapy, epigenetics, histone methyltransferase, immune evasion

The placenta is far more than a passive conduit for nutrients and oxygen. It is a highly regulated immunological interface, an organ that must tolerate a genetically distinct fetus while still defending both mother and child from infection. Resident macrophages, the immune cells that patrol placental tissue, are central to this balancing act. In their resting, anti-inflammatory M2 state, these cells promote immune tolerance, tissue remodeling, and healthy vascular development. When they shift into the pro-inflammatory M1 state, they mount antimicrobial responses but also unleash cytokines that can damage the very tissue they inhabit. A healthy pregnancy depends on keeping this polarity in check, and the new research shows that nanoplastic particles can tip the scales decisively toward inflammation.

To probe the risk, the team built a two-tier experimental strategy that combined animal and human models. In vivo, pregnant mice were exposed to polystyrene nanoplastics during gestation, allowing the researchers to examine placental toxicity in a living system where maternal circulation, fetal development, and immune signaling all interact. In parallel, the investigators developed an in vitro co-culture system pairing HTR8/SVneo cells, a widely used model of human extravillous trophoblasts, with macrophages derived from THP-1 human monocytic leukemia cells treated with phorbol ester to induce differentiation. This dual design let the researchers observe the consequences of exposure in intact placentas while dissecting the cellular mechanisms at single-cell-type resolution.

The first major finding emerged from RNA sequencing of placentas harvested from exposed mice. Transcriptomic analysis revealed significant enrichment of inflammatory response pathways, including the gene ontology term GO:0006954 and multiple associated KEGG signaling pathways. In plain terms, the exposed placentas looked inflamed at the level of their gene expression. Crucially, the researchers then confirmed that this inflammatory signature was accompanied by a measurable shift in macrophage polarization: the population of immune cells within placental tissue had moved toward the M1, pro-inflammatory phenotype, at the expense of the M2, anti-inflammatory state that normally predominates in a healthy pregnancy.

From the sequencing data, the team zeroed in on three differentially expressed genes linked to inflammation: ARG1, which encodes arginase 1, a hallmark enzyme of the M2 program; CCR5, a chemokine receptor involved in immune cell trafficking and inflammatory signaling; and IL1R2, a decoy receptor for the inflammatory cytokine interleukin-1. All three were carried forward for validation in the human cell system using RT-qPCR, a technique that quantifies gene expression with high sensitivity. In PMA-treated THP-1 macrophages exposed to the nanoparticles, ARG1 and CCR5 were consistently downregulated, while IL1R2 was upregulated. Immunohistochemistry on placental tissue corroborated the changes at the protein level.

Among the three candidate markers, only one behaved identically across every layer of evidence. ARG1 showed consistent downregulation at both the transcriptional level, detected independently by RNA sequencing and RT-qPCR, and the translational level, detected by immunohistochemistry. CCR5 and IL1R2, by contrast, did not maintain the same coherent pattern across all assays. This convergence convinced the researchers that ARG1 stands out as a robust and reliable indicator of nanoplastic-induced placental toxicity, a biomarker candidate that could prove valuable both for future mechanistic studies and, potentially, for monitoring real-world exposure effects.

The functional implications go deeper than correlation. Because arginase 1 is a defining effector molecule of the M2 program, its suppression effectively disarms the anti-inflammatory arm of placental macrophages. In the co-culture experiments, the researchers demonstrated that nanoplastic exposure suppressed the M2 anti-inflammatory phenotype while promoting the M1 pro-inflammatory phenotype, and that this polarization shift was driven by the inhibition of ARG1 expression. In other words, the particles do not simply provoke a generic inflammatory reaction; they reprogram immune cell identity by switching off a master regulator of the tolerance-promoting state. The macrophages themselves become agents of placental injury, releasing inflammatory signals in tissue that depends on calm for its function.

This mechanism helps explain how an environmental exposure could translate into developmental risk. An inflamed placenta is an inefficient placenta. Pro-inflammatory macrophage polarization has been implicated in a range of pregnancy complications, including preeclampsia, fetal growth restriction, and abnormal trophoblast invasion, and prior work by the same group linked nanoplastic exposure to ferroptosis, an iron-dependent form of cell death, in placental tissue through epigenetic mechanisms. The new findings add an immunological layer to that picture: even before cells die, the microenvironment around them is being pushed into a state that undermines nutrient exchange, vascular remodeling, and maternal-fetal immune tolerance, all of which are essential for normal fetal growth.

The study also arrives amid a rapidly expanding body of evidence that plastic particles penetrate the most protected compartments of the human body. Researchers have quantified microplastics in human placental specimens using pyrolysis gas chromatography mass spectrometry, detected them in maternal blood and umbilical vein blood, and traced their accumulation from placenta to fetal organs in animal models. Particle size matters as well: smaller nanoplastics cross biological barriers more readily than microplastics, and previous studies have shown that different particle sizes can differentially regulate pro-inflammatory macrophage polarization. What distinguishes the new work is that it moves beyond documenting the presence of these particles and identifies a specific molecular lever, ARG1, through which they exert their effect on a critical organ.

The researchers emphasize that their findings highlight a new risk factor for fetal development, one that arises from the collision between global plastic pollution and the immunological choreography of pregnancy. While the experiments were conducted in mouse models and human cell lines, the conserved biology of macrophage polarization and placental immune regulation suggests the mechanism is plausibly relevant to human pregnancies, particularly given the documented presence of plastics in human placentas. As nanoplastic contamination of air, food, and water continues to rise, the study underscores that the most vulnerable window of human development may be quietly exposed to particles capable of reprogramming the immune cells charged with protecting it. Identifying ARG1 as a consistent molecular signature of that exposure provides researchers with a concrete target for biomarkers, interventions, and, ultimately, a better understanding of how the modern material world shapes the earliest chapters of life.

Subject of Research: Effects of gestational polystyrene nanoplastic exposure on placental function and macrophage polarization

Article Title: Gestational polystyrene nanoplastic exposure impairs placental function via ARG1-associated macrophage polarization imbalance

Article References: Yujiao, C., Yifan, L., Shanshan, L., Wei, W., Meng, Z., & Yousheng, Y. (2026). Gestational polystyrene nanoplastic exposure impairs placental function via ARG1-associated macrophage polarization imbalance. Journal of Nanoparticle Research, 28(9), Article 242. https://doi.org/10.1007/s11051-026-06764-1

Image Credits: AI Generated

DOI: 10.1007/s11051-026-06764-1

Keywords: polystyrene nanoplastics, placental toxicity, macrophage polarization, ARG1, pregnancy, placenta, inflammation, fetal development, nanotoxicology, trophpoblast, HTR8/SVneo, immune tolerance