N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q), an emerging tire-derived environmental contaminant, is widely detected in airborne particles, raising concerns about its respiratory health effects. However, its role in asthma remains poorly understood. Here, we employed an integrated approach combining network toxicology, bioinformatics analyses, molecular docking, and in vivo validation to investigate the mechanisms of 6PPD-Q in asthma. Network toxicology analysis identified 374 shared targets between 6PPD-Q and asthma that were enriched in inflammatory and immune-related pathways, including chemokine, NF-κB, and IL-17 signaling. Protein-protein interaction analysis further identified 10 hub genes within the target network. Validation using the GSE143303 dataset demonstrated that these hub genes were predominantly associated with neutrophilic asthma, characterized by increased expression of CCL2, CXCL8, and CXCL10. Integration of neutrophilic asthma-related differentially expressed genes with network-derived targets, followed by least absolute shrinkage and selection operator (LASSO) regression, identified seven key genes, with CXCL8, C2, and FGR significantly upregulated. Immune infiltration analysis suggested close associations between these genes and innate immune cell responses. Molecular docking revealed a strong predicted interaction between 6PPD-Q and FGR, with a binding energy of -8.6 kcal/mol. In vivo, 6PPD-Q exposure alone elicited mild pulmonary inflammation in non-asthmatic mice. In mice with neutrophilic asthma, 6PPD-Q further increased airway inflammation and hyperresponsiveness, whereas no significant additional changes were observed in mice with eosinophilic asthma. These effects were accompanied by increased pulmonary FGR expression and activating phosphorylation of Src-family kinases. Collectively, 6PPD-Q exerts intrinsic pro-inflammatory effects but preferentially exacerbates neutrophilic asthma, with FGR representing a candidate mediator warranting functional validation.

Allergic asthma is associated with a reduction in the number of regulatory T cells (Tregs). Although interleukin-27 (IL-27) has been shown to modulate Tregs potentially through the Lymphocyte-activation gene 3 (Lag3) pathway, the underlying mechanism remains incompletely defined. Objective: This study sought to determine whether IL-27 ameliorates airway inflammation in asthma by modulating Tregs in a Lag3-dependent manner. Acute asthma was induced in wild-type (WT) and Lag3 knockout (Lag3-/-) mice through sensitization and challenge with house dust mite (HDM). A treatment group received intranasal recombinant IL-27 prior to challenges. In WT mice, IL-27 administration significantly attenuated airway inflammation, goblet cell hyperplasia, and total cell counts in bronchoalveolar lavage fluid (BALF), along with reduced levels of Th2 cytokines (IL-4, IL-5). It also upregulated T-bet (Th1) mRNA expression, downregulated GATA-3 (Th2) and RORγt (Th17) levels, and increased the proportions of CD4+ Foxp3+ Tregs, CTLA4+ Tregs, and Lag3+ Tregs in lung tissue. Conversely, in Lag3-/- mice, the protective effects of IL-27 were completely abrogated, with no observed increases in Treg populations or suppression of Th2/Th17 immune responses. The anti-asthmatic effect of exogenous IL-27 is associated with increased Treg frequency and upregulation of inhibitory markers, with Lag3 serving as a pivotal target on Tregs.

Objective: To delineate the demographic, clinical, and radiological features of immunocompetent patients with pulmonary cryptococcosis (PC) who test negative for serum cryptococcal antigen (CrAg), a subgroup that poses a diagnostic challenge. Methods: Participants were stratified into CrAg-positive (n = 128) and CrAg-negative (n = 71) cohorts. Comparative analyses were performed on clinical presentation, chest computed tomography (CT) imaging features, and laboratory parameters. Results: Patients with false-negative CrAg results were more likely to be asymptomatic (46.5% vs. 20.3% in the CrAg-positive group; p < 0.05). Their chest CT scans typically revealed solitary pulmonary nodules, frequently unilateral and located in the right lung, with a notable absence of pleural effusion or lymphadenopathy. Laboratory findings in the CrAg-negative group were characterized by a lower neutrophil ratio and erythrocyte sedimentation rate. Furthermore, higher CrAg titers were significantly correlated with the presence of respiratory symptoms, specific CT signs (e.g., air bronchogram, lymphadenopathy), and elevated systemic inflammatory markers. Conclusions: False-negative serum CrAg in immunocompetent PC patients is characterized by an asymptomatic presentation and a solitary nodule on imaging, with normal laboratory parameters. CrAg titers may reflect disease severity and warrant prospective evaluation as a potential biomarker for guiding antifungal therapy.

Lung ischemia-reperfusion injury (LIRI) is a serious complication in critical clinical situations. Despite its importance, the specific role of type II natural killer T (NKT) cells in LIRI remains unclear. In this study, we establish a LIRI mouse model and demonstrate that sulfatide-reactive type II NKT cells promote M2 polarization of alveolar macrophages (AMs) and alleviate LIRI through AMs-mediated mechanisms. This protective effect is absent in Jα18−/- mice, indicating the essential role of invariant NKT (iNKT) cells. Further analysis shows that interleukin-10 (IL-10) secreted by iNKT cells upregulates AT-rich interaction domain 3 A (Arid3a) in macrophages, which then promotes the transcription of DNA damage inducible transcript 4 (DDIT4). This cascade enhances M2 polarization of macrophages, potentially contributing to lung protection and alleviating LIRI. These findings suggest that NKT cells may offer a therapeutic target for LIRI in the future. Mechanistic modeling of sulfatide-reactive type II NKT cells reveals their role in regulating M2 polarization of alveolar macrophages through the iNKT cell–IL-10 axis, thereby alleviating lung ischemia–reperfusion injury.

Background:Lung transplantation is the only effective therapeutic option for patients with end-stage lung disease. However, ischemia/reperfusion injury (IRI) during transplantation is a leading cause of primary graft dysfunction (PGD). Ferroptosis, a form of iron-dependent cell death driven by lipid peroxidation, has been implicated in IRI across various organs. This study aims to explore the role of ferroptosis in lung transplantation-related ischemia/reperfusion injury and to identify its potential molecular mechanisms through bioinformatics analysis. Methods:Transcriptome data from lung transplant patients were obtained from the Gene Expression Omnibus (GEO) database. Ferroptosis-related differentially expressed genes (FRGs) were identified by analyzing gene expression profiles before and after reperfusion. Weighted gene co-expression network analysis (WGCNA) was used to identify module genes, and overlapping genes were further analyzed using two machine learning algorithms. The CIBERSORT algorithm was applied to assess immune cell infiltration, while Mendelian randomization (MR) analysis was used to investigate causal relationships between candidate genes and PGD. Finally, Consensus clustering based on FRGs was performed to identify subtypes. Results:We identified four candidate genes associated with ferroptosis during lung reperfusion: tumor necrosis factor alpha-induced protein 3 (TNFAIP3), C-X-C motif chemokine ligand 2 (CXCL2), neural precursor cell expressed developmentally down-regulated 4-like (NEDD4L), and sestrin 2 (SESN2). These genes were closely associated with immune cell infiltration. MR analysis suggested that SESN2 might play a protective role against PGD. Additionally, consensus clustering revealed distinct immune infiltration patterns across subtypes, providing insights for personalized therapeutic approaches to lung ischemia/reperfusion injury (LIRI). Conclusion:This study highlights TNFAIP3, CXCL2, NEDD4L, and SESN2 as candidate genes associated with ferroptosis during LIRI, with SESN2 potentially protecting against PGD. These findings offer promising therapeutic targets for preventing LIRI and improving outcomes in lung transplantation.

This study aims to explore the association between anoikis-related genes (ARGs) and asthma. The dataset GSE143303 for asthma were sourced from the GEO database, while ARGs were retrieved from the Harmonizome web portal and the GeneCards database. Differentially expressed genes (DEGs) identification and GO, KEGG enrichment analysis were performed to reveal potential biological pathways. To identify hub anoikis-related DEGs (hub ARDEGs), we employed WGCNA and machine learning methods including LASSO and Random Forest. Additionally, we constructed risk prediction nomogram model and ROC curves to evaluate the asthma diagnostic value of hub ARDEGs. SsGSEA immune infiltration analysis was used to analyze the role of hub ARDEGs in the asthma immune microenvironment. Finally, miRNAs and transcription factors (TFs) interacting with these hub ARDEGs were investigated. DEGs of ARGs between asthma and healthy controls, along with WGCNA, led to the identification of six ARDEGs. GO and KEGG analyses revealed that these ARDEGs were primarily involved in the apoptotic signaling pathway and adherens junctions. Machine learning methods further narrowed down the six ARDEGs to two hub ARDEGs: PARP1 and SDCBP, which were significantly upregulated in asthma and validated using the GSE147878 and experimental models. Based on these two hub ARDEGs, a risk prediction model for asthma was developed, demonstrating strong diagnostic potential and tissue specificity in endobronchial biopsies. Immune analysis revealed variations in immune cell infiltration within asthma samples correlated with hub ARDEGs. Additionally, the miRNA-TF-mRNA interaction network of hub ARDEGs highlights the complexity of the regulatory process. The process of anoikis, immune dysregulation, and asthma are closely interconnected. The anoikis-related biomarkers PARP1 and SDCBP may serve as diagnostic markers and therapeutic targets for asthma.

Radiolucent foreign body aspiration (FBA) remains diagnostically challenging due to its subtle imaging signatures on chest CT scans, often leading to delayed or missed diagnoses. We present a deep learning model integrating MedpSeg, a high-precision airway segmentation method, with a convolutional classifier to detect radiolucent FBA. The model was trained and validated across three independent cohorts, demonstrating consistent performance with accuracies above 90% and balanced recall-precision metrics. In a blinded independent evaluation cohort, the model outperformed expert radiologists in both recall (71.4% vs. 35.7%) and F1 score (74.1% vs. 52.6%), highlighting its potential to reduce missed cases (false negatives) and support clinical decision-making. This study illustrates the translational potential of artificial intelligence for addressing diagnostically complex and high-risk conditions, offering an effective tool to support radiologists in the assessment of suspected radiolucent foreign body aspiration. Code is available at https://github.com/ZheChen1999/FBA_DL .

BACKGROUND:Preserved ratio impaired spirometry (PRISm) is associated with asthma. However, it is unclear whether PRISm increases the risk of mortality in non-smoking asthma patients compared with normal spirometry. METHODS:This prospective cohort study included 748 adult asthma participants with no smoking history and no airflow obstruction at baseline. Participants were divided into two groups: normal spirometry (FEV1 ≥ 80% predicted) and PRISm (FEV1 < 80% predicted). The median follow-up time was 9.6 years. Multivariable Cox regression analyses and Kaplan-Meier survival were used to assess the association between PRISm and all-cause mortality. All analyses took into account the complex survey design. RESULTS:At baseline, 8.52% of participants exhibited PRISm. Multivariable Cox regression analysis showed that PRISm was independently associated with all-cause mortality after adjusting for confounding factors (adjusted hazard ratio = 6.57, 95% CI: 2.33-18.47, p < 0.001). Kaplan-Meier survival analysis showed that the survival rate in the PRISm group was significantly worse than that in the normal spirometry group (log-rank test p = 0.006). In a sensitivity analysis excluding participants with possible restrictive spirometry, this association remained with almost the same effect size (adjusted hazard ratio = 6.99, 95% CI: 1.67-29.29, p = 0.008). CONCLUSIONS:In asthma patients with no smoking history and no airflow obstruction at baseline, PRISm was significantly associated with an increased risk of all-cause mortality during follow-up. However, this result needs to be interpreted with caution due to the wide confidence intervals.

Severe asthma is a significant health concern due to its association with higher mortality rates, reduced quality of life, and increased healthcare costs. These challenges make it a persistent issue for both clinicians and researchers. The small airways, defined as distal airways with a diameter of less than 2 mm and comprising 98.8% of the total lung volume, play a significant role in airway resistance in individuals with asthma. Recent studies demonstrated that small airways dysfunction is found in all asthma severity levels, but it is most pronounced in severe asthma, and greater small airways dysfunction severity correlates with poorer asthma control and a higher frequency of exacerbations. Therefore, therapies aimed at targeting small airways dysfunction are essential for effective asthma management, especially in severe asthma.

ABSTRACT Background Tuberculous pericarditis begins with fibrinous and hemorrhagic pericarditis, followed by pericardial effusion, then pericardial hypertrophy, which may turn into subacute or chronic stage, and partly develop into pericarditis. Early diagnosis and treatment have very important clinical significance. Case Summary We present a case of an 82‐year‐old man with a known history of hypertension who was admitted for pleural effusion. CT scan of the chest showed findings of pleural effusion. An echocardiographic study during admission revealed a small amount of pericardial effusion (~1.2 cm in thickness). A whole‐body positron emission tomography‐computer tomography (PET‐CT) scan was then performed and showed a slightly increased fluorodeoxyglucose uptake in the entire pericardium considering tuberculosis. He was started on antituberculosis (TB) medications and tolerated them well. Follow‐up echocardiographic study showed no re‐accumulation of pleural effusion and pericardial fluid. Conclusion Transudative–exudative pleural effusion may be one of the clinical manifestations of tuberculous pericarditis. (1) Bilateral leaking pleural effusion may be the early clinical manifestation of tuberculous pericarditis; (2) PET/CT in the diagnosis and efficacy evaluation of tuberculous pericarditis is valuable; and (3) the central venous pressure may be an indicator of choice for treatment of tuberculous pericarditis.

BACKGROUND:Lung ischemia/reperfusion injury (LIRI) is a common occurrence in clinical practice and represents a significant complication following pulmonary transplantation and various diseases. At the core of pulmonary ischemia/reperfusion injury lies sterile inflammation, where the innate immune response plays a pivotal role. This review aims to investigate recent advancements in comprehending the role of innate immunity in LIRI.METHODS:A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning lung ischemia/reperfusion injury, cell death, damage-associated molecular pattern molecules (DAMPs), innate immune cells, innate immunity, inflammation.RESULTS:During the process of lung ischemia/reperfusion, cellular injury even death can occur. When cells are injured or undergo cell death, endogenous ligands known as DAMPs are released. These molecules can be recognized and bound by pattern recognition receptors (PRRs), leading to the recruitment and activation of innate immune cells. Subsequently, a cascade of inflammatory responses is triggered, ultimately exacerbating pulmonary injury. These steps are complex and interrelated rather than being in a linear relationship. In recent years, significant progress has been made in understanding the immunological mechanisms of LIRI, involving novel types of cell death, the ability of receptors other than PRRs to recognize DAMPs, and a more detailed mechanism of action of innate immune cells in ischemia/reperfusion injury (IRI), laying the groundwork for the development of novel diagnostic and therapeutic approaches.CONCLUSIONS:Various immune components of the innate immune system play critical roles in lung injury after ischemia/reperfusion. Preventing cell death and the release of DAMPs, interrupting DAMPs receptor interactions, disrupting intracellular inflammatory signaling pathways, and minimizing immune cell recruitment are essential for lung protection in LIRI.

Our previous studies have showed that sulfatide-reactive type II NKT (i.e. variant NKT, vNKT) cells inhibit the immunogenic maturation during the development of mature lung dendritic cells (LDCs), leading todeclined allergic airway inflammation in asthma. Nonetheless, the specific immunoregulatory roles of vNKT cells in LDC-mediated Th2 cell responses remain incompletely understood. Herein, we found that administration of sulfatide facilitated the generation of CD4+FoxP3+ regulatory T (Treg) cells in the lungs of wild-type mice, but not in CD1d-/- and Jα18-/- mice, after ovalbumin or house dust mite exposure. This finding implies that the enhancement of lung Treg cells by sulfatide requires vNKT cells, which dependent on invariant NKT (iNKT) cells. Furthermore, the CD4+FoxP3+ Treg cells induced by sulfatide-reactive vNKT cells were found to be associated with PD-L1 molecules expressed on LDCs, and this association was dependent on iNKT cells. Collectively, our findings suggest that in asthma-mimicking murine models, sulfatide-reactive vNKT cells facilitate the generation of lung Treg cells through inducing tolerogenic properties in LDCs, and this process is dependent on the presence of lung iNKT cells. These results may provide a potential therapeutic approach to treat allergic asthma.

Recent studies have shown that cellular senescence is involved in the pathogenesis of severe asthma (SA). The objective of this study was to investigate the role of cellular senescence-related genes (CSGs) in the pathogenesis of SA. Here, 54 differentially expressed CSGs were identified in SA patients compared to healthy control individuals. Among the 54 differentially expressed CSGs, 3 CSGs (ETS2, ETS1 and AURKA) were screened using the LASSO regression analysis and logistic regression analysis to establish the CSG-based prediction model to predict severe asthma. Moreover, we found that the protein expression levels of ETS2, ETS1 and AURKA were increased in the severe asthma mouse model. Then, two distinct senescence subtypes of SA with distinct immune microenvironments and molecular biological characteristics were identified. Cluster 1 was characterized by increased infiltration of immature dendritic cells, regulatory T cells, and other cells. Cluster 2 was characterized by increased infiltration levels of eosinophils, neutrophils, and other cells. The molecular biological characteristics of Cluster 1 included aerobic respiration and oxidative phosphorylation, whereas the molecular biological characteristics of Cluster 2 included activation of the immune response and immune receptor activity. Then, we established an Random Forest model to predict the senescence subtypes of SA to guide treatment. Finally, potential drugs were searched for each senescence subgroup of SA patients via the Connectivity Map database. A peroxisome proliferator-activated receptor agonist may be a potential therapeutic drug for patients in Cluster 1, whereas a tachykinin antagonist may be a potential therapeutic drug for patients in Cluster 2. In summary, CSGs are likely involved in the pathogenesis of SA, which may lead to new therapeutic options for SA patients.

Background B cells were believed to act as antigen-presenting cells (APCs) to promote T helper type 2 (Th2) cell responses. However, the role of lung B cells and its subpopulations in Th2 cell responses in asthma remains unclear. Objective We leveraged an anti-CD20 monoclonal antibody (mAb) treatment that has been shown to selectively deplete B cells in mice and investigated whether this treatment modulates Th2 cell responses and this modulation is related to lung follicular mature (FM) B cells in a murine model of asthma. Methods and results We used a house dust mite (HDM)-induced asthma mouse model and found that anti-CD20 mAb treatment attenuates Th2 cell responses. Meanwhile, anti-CD20 mAb treatment did dramatically reduce the number of B cells, especially FM B cells in the lungs, but did not impact the frequency of other immune cell types, including lung T cells, dendritic cells, natural killer cells, and regulatory T cells in wild-type mice. Moreover, we found that the suppressive effect of anti-CD20 mAb treatment on Th2 cell responses could be reversed upon adoptive transfer of lung FM B cells, but not lung CD19 + B cells without FM B cells in asthmatic mice. Conclusions These findings reveal that anti-CD20 mAb treatment alleviates Th2 cell responses, possibly by depleting lung FM B cells in a Th2-driven asthma model. This implies a potential therapeutic approach for asthma treatment through the targeting of lung FM B cells.

Invariant natural killer T cells(iNKT), also called as type I NKT cells, are a natural subset of T cells that can recognize lipid antigens presented by CD1d molecules. By expressing different surface markers or transcription factors, iNKT cells can be separated into different subgroups. iNKT subsets play important roles in protection from infection, regulating tumor and inflammation immunity as well as maintaining the tissue homeostasis. While activated iNKT cell subsets are also involved in the pathogenesis of some diseases. This review mainly discussed the phenotypical and functional properties of iNKT subsets divided based on the surface markers or the transcription factors.

G protein-coupled receptor kinase-2 (GRK2) is involved in TGF-β1-induced activation of lung fibroblasts, which could give rise to the pathogenesis of pulmonary fibrosis. Paroxetine (PRXT) serves as a selective GRK2 inhibitor which is widely used to treat anxiety and depression for several decades. However, whether PRXT could inhibit TGF-β1-induced activation of lung fibroblasts and combat bleomycin-induced pulmonary fibrosis remains unclear. Here, we investigated the effects of PRXT on pulmonary fibrosis in C57/BL6 caused by bleomycin as well as on the activation of murine primary lung fibroblasts stimulated with TGF-β1. The results demonstrated that PRXT markedly improved the pulmonary function and 21-day survival in bleomycin-induced mice. Meanwhile, PRXT significantly decreased collagen deposition, inflammation, and oxidative stress in lung tissues from bleomycin-induced mice. Furthermore, we found that PRXT could inhibit the protein and mRNA expression of GRK2 and Smad3 in lung tissues from bleomycin-induced mice. In vitro experiments also PRXT could inhibit cell activation and collagen synthesis in a concentration-dependent manner in TGF-β1-induced lung fibroblasts. In addition, we found that Smad3 overexpression by adenovirus transfection could offset anti-fibrotic and antioxidative effects from PRXT in TGF-β1-induced lung fibroblasts, which showed no effects on the protein expression of GRK2. In conclusion, PRXT mediates the inhibition of GRK2, which further blocks the transcription of Smad3 in TGF-β1-induced lung fibroblasts, providing an attractive therapeutic target for pulmonary fibrosis.

To the Editor Asthma is a chronic airway inflammatory disorder characterized by airway hyperresponsiveness and reversible airflow limitation.1 Never-theless,not every reversible airflow limitation is asthma.In this letter,we aim to describe the definition of reversible airflow limitation and the differences in airway diseases with reversible airflow limitation.

Abstract Background Infections with fungi, such as Aspergillus species, have been found as common complications of viral pneumonia. This study aims to determine the risk factors of fungal superinfections in viral pneumonia patients using meta‐analysis. Objective This study aims to determine the risk factors of fungal infection s in viral pneumonia patients using meta‐analysis. Methods We reviewed primary literature about fungal infection in viral pneumonia patients published between January 1, 2010 and September 30, 2020, in the Chinese Biomedical Literature, Chinese National Knowledge Infrastructure, Wanfang (China), Cochrane Central Library, Embase, PubMed, and Web of Science databases. These studies were subjected to an array of statistical analyses, including risk of bias and sensitivity analyses. Results In this study, we found a statistically significant difference in the incidence of fungal infections in viral pneumonia patients that received corticosteroid treatment as compared to those without corticosteroid treatment (p < .00001). Additionally, regarding the severity of fungal infections, we observed significant higher incidence of invasive pulmonary aspergillosis (IPA) in patients with high Acute Physiology and Chronic Health Evaluation (APACHE) II scores (p < .001), tumors (p = .005), or immunocompromised patients (p < .0001). Conclusions Our research shows that corticosteroid treatment was an important risk factor for the development of fungal infection in patients with viral pneumonia. High APACHE II scores, tumors, and immunocompromised condition are also important risk factors of developing IPA. The diagnosis of fungal infection in viral pneumonia patients can be facilitated by early serum galactomannan (GM) testing, bronchoalveolar lavage fluid Aspergillus antigen testing, culture, and biopsy.

Our previous findings show that invariant natural killer T (iNKT)cells can promote immunogenic maturation of lung dendritic cells (LDCs) to enhance Th2 cell responses in asthma. It has been accepted that recognition of glycolipid antigens presented by CD1d molecules by the T cell receptors of iNKT cells leads to iNKT cell activation. Therefore, we examine the immunoregulatory influences of anti-CD1d treatment on Th2 cell response and immunogenic maturation of LDCs and subsequently explored whether these influences were dependent on lung iNKT cells in asthmatic mice. We discoveredthat in wild-type mice sensitized and challenged with house dust mite or ovalbumin (OVA), anti-CD1d treatment inhibited Th2 cell response and immunogenic maturation of LDCs. LDCs from asthmatic mice with anti-CD1d treatment had a markedly decreased influence on Th2 cell responses in vivo and in vitro. Furthermore, anti-CD1d treatment reduced the abundance and activation of lung iNKT cells in asthmatic mice. Moreover, in asthmatic iNKT cell-deficient Jα18-/- mice, anti-CD1d treatment did not influence Th2 cell responses and immunogenic maturation of LDCs. Meanwhile, the quantity of CD40L+ iNKT cells in asthmatic mice was significant decreased by anti-CD1d treatment. Finally, the inhibition of anti-CD1d treatment on LDC immunogenic maturation and Th2 cell responses in asthmatic mice was reversed by anti-CD40 treatment. Our data suggest that anti-CD1d treatment can suppress Th2 cell responses through inhibiting immunogenic maturation of LDCs dependent on lung iNKT cells, which couldbe partially related to the downregulation of CD40L expression on lung iNKT cells in asthmatic mice.

Interleukin (IL)-27 is a heterodimeric cytokine composed by IL-27p28 and EBI3 subunits, belonging to the IL-6 and IL-12 cytokine families. IL-27 is mainly derived from antigen-presenting cells(APC), and takes part in innate and adaptive immune responds. Recently it has been found that IL-27 mainly exerts potent immune effects, regulating helper T cell (Th)1 differentiation, strengthening immune activity of CD4 + T and CD8 + T cells, or directly inhabiting tumor growth. Based on the structure, biological function and signaling pathway of IL-27, this review summarizes the anti-tumor mechanism of IL-27 and new research advances in different cancers.