31 May 2026, Volume 46 Issue 3

    

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  The heterogeneity and targeting strategies of tumor-associated macrophages

  LI Tao, WANG Xinyu, SONG Hongrui, CHEN Jun

  Current Immunology. 2026, 46(3): 269-286.

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  Tumor-associated macrophages (TAMs) represent the most abundant immune cell subset within the tumor microenvironment (TME) and play a critical role in tumor progression by diverse mechanisms. The advent of single-cell omics technologies has enabled the fine-resolution analysis of TAM heterogeneity and plasticity. Notably, TAMs exhibit dynamic and context-dependent phenotypic and functional characteristics across different cancer types and at various stages of tumor evolution. While immunotherapies centered on adaptive immunity have achieved certain progress in recent years, they also face significant limitations. TAMs are now recognized as key drivers of tumor immune evasion, spurring growing interest in the development of related targeting strategies. This review systematically elaborates on the heterogeneity in the origin and function of TAMs and provides a comprehensive overview of current therapeutic strategies and drug development progress targeting TAMs, aiming to offer theoretical foundations and novel perspectives for overcoming the current bottlenecks in immunotherapy.
  

  
  
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  Baicalin protects allergic rhinitis rats by maintaining the Th1/Th2 balance

  WANG Yuxia, CHEN Jinghua, WANG Dan

  Current Immunology. 2026, 46(3): 287-294.

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  This study aims to investigate the protective effects of baicalin (BA) on allergic rhinitis (AR) rats, as well as its regulation on immune and the underlying molecular mechanisms. The AR rat model was established by intraperitoneal injection and nasal administration of ovalbumin （OVA). The AR rats were divided into the AR group, the low BA group (50 mg/kg BA), the high BA group (200 mg/kg BA) and the high BA +phorbol myristate acetate （PMA） group (200 mg/kg BA+5 mg/kg PMA), and untreated SD rats were used as the control group, with 10 rats in each group. For each group, rhinitis symptom score were evaluated, serum IgE and histamine levels were detected by ELISA, eosinophils in nasal lavage fluid were detected by Diff-Quik staining, pathological changes of nasal mucosa were detected by H-E staining, mast cell changes in nasal mucosa were detected by toluidine blue staining, and Th1/Th2 cells in peripheral blood of rats were detected by flow cytometry. Western blotting was used to measure protein expressions of IFN-γ, IL-2, IL-4, TLR4, p-NF-κB p65 and NF-κB p65. The results showed that in the AR group, the nasal mucosa thickened, mast cell infiltration increased, and goblet cell lesions were obvious. BA treatment alleviated the degree of nasal mucosal tissue lesions in AR rats. Compared to those of the AR group, BA treatment significantly lowered the rhinitis score, IgE and histamine levels, eosinophil count, and Th2 proportion (P<0.05), while  markedly increased Th1 proportion and the Th1/Th2 ratio (P<0.05). BA also significantly reduced the protein levels of IL-4, TLR4 and p-NF-κB p-65 in the nasal mucosa (P<0.05) and increased IL-2 and IFN-γ levels (P<0.05). PMA treatment partially reversed the protective effect of high-dose BA in AR rats. The results show that BA exerts a protective effect in AR rats, likely by maintaining Th1/Th2 balance and inhibiting activation of the TLR4/NF κB signaling pathway.
  

  
  

  
  
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  miR-145-5p targets SOX2 to regulate the Wnt/β-catenin signaling pathway, inhibiting the proliferation, metastasis, and angiogenesis of non-small cell lung cancer

  LIU Zeyu, SONG Shiwei

  Current Immunology. 2026, 46(3): 295-305.

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  Lung cancer is a leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) being the most common type. miR-145-5p has been shown to have tumor-suppressive effects in several types of cancer. However, its role in NSCLC is not fully understood. This study aims to explore the effects of miR-145-5p on the malignant progression and angiogenesis of NSCLC, along with its potential mechanisms. First, the expression levels of miR-145-5p and SRY-box transcription factor 2 (SOX2) in NSCLC cells were detected using qRT-PCR or Western blotting. The effects of miR-145-5p on NSCLC cell proliferation, migration, invasion, and angiogenesis were evaluated using CCK-8, Transwell assay, and angiogenesis analysis. A tumor xenograft model was constructed to determine the impact of miR-145-5p on the in vivo growth and angiogenesis of NSCLC. The direct targeting relationship between miR-145-5p and SOX2 was validated using dual-luciferase reporter assay. The results indicated that miR-145-5p was significantly downregulated in NSCLC cell lines, and it inhibited NSCLC proliferation and angiogenesis both in vitro and in vivo. Further studies revealed that SOX2 is a downstream target gene of miR-145-5p, which activated the Wnt/β-catenin signaling pathway. miR-145-5p modulated the Wnt/β-catenin pathway by targeting and inhibiting the expression of SOX2, thereby suppressing NSCLC cell proliferation, migration, invasion, and angiogenesis. These findings suggest that miR-145-5p may be a potential therapeutic target for NSCLC.
  

  
  

  
  
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  Correlation between TLR4 expression and intestinal flora diversity in acute pancreatitis patients

  YU Kejing, QIU Zhixin, WANG Zhibing, JIA Shihao, ZHANG Manhe

  Current Immunology. 2026, 46(3): 306-312.

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   The study aims to investigate the correlation between TLR4 expression and intestinal flora diversity in acute pancreatitis patients. A total of 116 acute pancreatitis patients were selected as the study object. 5 mL of whole blood from cubital vein was extracted from patients when enrolled. Peripheral blood monocytes were separated by density gradient centrifugation and total RNA was extracted to evaluate the relative expression of TLR4 mRNA. According to the dichotomy of TLR4 mRNA expression level, 58 cases were classified into the high expression group (≥1.26, A group) and 58 cases were classified into the low expression group (＜1.26, B group). Clinical data of the two groups were compared. Fecal samples of the two groups were collected and subjected to 16S rRNA sequencing to analyze the intestinal flora. Bacterial abundance (Chao1 index and ACE index) and diversity (Shannon index and Simpson index) were evaluated respectively. The species with significant intergroup differences were selected by LEfSe analysis, and the correlation between TLR4 mRNA expression level and intestinal flora diversity was further evaluated by Pearson correlation analysis. The results showed that there were 198 species unique to group A, 268 species unique to group B, and 374 species shared by the two groups according to 16S rRNA sequencing. The Chao1 index, ACE index, and Shannon index of group A were significantly lower than those of group B, while Simpson index was significantly higher (P<0.05). LEfSe analysis revealed a significant enrichment of opportunistic pathogens  in group A, including Enterococcus faecalis, Escherichia coli, and Enterococcus faecium, whereas group B exhibited significant enrichment of probiotic or anti-inflammatory bacteria such as Prevotella, Akkermansia, Bifidobacterium, and Faecalibacterium prausnitzii. Pearson correlation analysis demonstrated that TLR4 mRNA expression was negatively correlated with the Chao1 index, ACE index, Shannon index, Prevotella, Akkermansia, Bifidobacterium,and Faecalibacterium prausnitzii(P<0.05), while positively correlated with the Simpson index, Enterococcus faecalis, Escherichia coli, and Enterococcus faecium (P<0.05). The study suggests that TLR4 expression in acute pancreatitis patients is closely related to the diversity and composition of their intestinal flora. And that the high expression of TLR4 is associated with the decrease of intestinal flora abundance and diversity, along with decrease of probiotics and enrichment of opportunistic pathogens.
  

  
  
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  Resolution of acute respiratory distress syndrome/acute lung injury by reversing the imbalance of Th17/Treg cells via protein kinase C theta targeting

  AO Jinxi, LUO Fuping, QIN Bao, MO Lin, WEI Qiulian, CHEN Renfa, LI Mengqin

  Current Immunology. 2026, 46(3): 313-318.

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   Studies have shown that CD4+CD25+ Treg exerts protective effect in acute respiratory distress syndrome (ARDS)/acute lung injury (ALI), whereas Th17 primarily plays a pro-inflammatory role. An imbalance in the Th17/Treg ratio is observed in various inflammatory and autoimmune diseases. Protein kinase C theta (PKCθ) is essential for Th17 cell differentiation and the suppression of Treg cell function. Therefore, this study hypothesizes that inhibiting PKCθ may alleviate ARDS/ALI by modulating the Th17/Treg ratio. Male C57BL/6 mice were treated with PBS, LPS, or LPS combined with a PKCθ inhibitor (PI), respectively. CD4+T cells were treated with PBS or PI. Bronchoalveolar lavage fluid (BALF) was examined for neutrophil count and TNF-α levels. Lung tissues were assessed for lung injury score, wet to dry weight ratio (W/D), and Th17/Treg ratio.The protein and mRNA expression of forkhead box P3(Foxp3) in lung tissue and CD4+ T cells were tested. Results showed that PKCθ inhibition markedly reduced the Th17/Treg ratio in lungs of ARDS mice. The Th17/Treg ratio positively associated with lung-injury scores, W/D of the lungs, neutrophil counts, TNF-α production in bronchoalveolar lavage fluid (BALF), and myeloperoxidase activity in lung tissue. Following PKCθ inhibition, the protein and mRNA levels of Foxp3 increased both in vivo and in vitro. Collectively, these data demonstrated that PKCθ inhibition protects against LPS-induced ARDS/ALI by reversing the Th17/Treg cell imbalance.
  

  
  
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  Effect of gut microbiota dysbiosis on inflammatory factors in colorectal cancer

  QIAO Pu, LIU Ju

  Current Immunology. 2026, 46(3): 319-326.

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   To investigate the impact of gut microbiota dysbiosis on the levels of inflammatory factors in colorectal cancer, patients diagnosed from April 2022 to November 2023 were selected based on inclusion and exclusion criteria, resulting in a total of 30 eligible cases. Normal tissue, tumor-adjacent tissue, and tumor tissue samples were collected from each patient. PCR was used to detect and analyze the gut microbiota and inflammatory factor levels in different tissue samples. The results showed thet among the selected patients, males accounted for 56% of the total. The inflammatory factor levels in normal tissue were as follows: IFN-β (37.68±4.88) pg/mL, TNF-α (624.35±34.68) pg/mL, and IL-6 (77.85±18.44) pg/mL. In tumor tissue, the levels were: IFN-β (62.48±4.68) pg/mL, TNF-α (1 245.58±20.51) pg/mL, and IL-6 (174.84±18.63) pg/mL. Significant differences were observed in the relative abundances of Firmicutes, Bacteroidetes, and Proteobacteria between cancerous and normal tissues (P<0.05). The composition of gut microbiota differs markedly between tumor and normal tissues in colorectal cancer patients, suggesting that gut microbiota dysbiosis may influence the expression of inflammatory factors and contribute to the carcinogenesis of normal tissue.
  

  
  
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  Expression of HOXC10 and MTFR2 in laryngeal squamous cell carcinoma and the clinical significance

  CHEN Yun, ZHANG Kai, ZHU Yuanzhi, LUO Jian, WANG Jianhong

  Current Immunology. 2026, 46(3): 336-341.

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  The study aims to analyze the expression and clinical significance of homeobox C10 (HOXC10) and mitochondrial fission regulator 2 (MTFR2)  in laryngeal squamous cell carcinoma. Sixty-two pathological specimens of laryngeal squamous cell carcinoma were selected as the research group, with normal specimens at the pathological margin serving (adjacent non-cancerous tissue) as the control group for this study. Immunohistochemistry was used to detect the expression of HOXC10 and MTFR2 in the tissues of both groups, and the relationship between their expression and pathological parameters was analyzed. Based on follow-up data, the correlation between their expression and patient prognosis was also analyzed. The results showed that the  positive expressions of HOXC10 and MTFR2 in cancer tissue were significantly higher than those in adjacent non-cancerous tissue (P<0.05). Spearman's rank correlation analysis showed that the expression of HOXC10 and MTFR2 was positively correlated (r=0.463， P<0.05). Among the clinical parameters of TNM stage, lymph node metastasis, clinical stage and pathological differentiation, the expressions of HOXC10 and MTFR2 were statistically significant (P<0.05). All patients were followed up for 3 to 60 months, and the deadline was August 2023. Among the 62 patients  followed up, 14 patients had recurrence, and the recurrence rate was 22.6%. In 1 year, 3 years and 5 years, the overall survival rates of all samples were 95.2%, 79.0% and 54.8% respectively. The overall survival rate of patients with positive expression of HOXC10 was 41.3%, while that of patients with negative expression of HOXC10 was 93.8%. The overall survival rate of patients with positive expression of MTFR2 was 43.6%, while that of patients with negative expression of MTFR2 was 73.9%. The Log-rank χ2 test revealed a significant survival rate difference between the two groups (P<0.05). By incorporating some indicators into the Cox regression model, the result showed that HOXC10 was an independent risk factor of prognostic survival (P=0.028). This study suggests that the HOXC10 and MTFR2 exhibit significantly high expressions in laryngeal squamous cell carcinoma and have a close relationship with patient prognosis.
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  Knockdown of Panx1 inhibits p38 MAPK to alleviate inflammatory injury and necroptosis of cardiomyocytes induced by OGD/R

  LI Caiyun, HUO Liwei, YAO Jie

  Current Immunology. 2026, 46(3): 342-349.

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  This study investigates the role of pannexin 1 (Panx1) in regulating p38 MAPK signaling and its impact on cardiomyocyte necroptosis following oxygen-glucose deprivation/reoxygenation (OGD/R). By analyzing myocardial ischemia/reperfusion injury (MI/RI) datasets (GSE160516 and GSE153493), differentially expressed genes (DEGs) were identified. Panx1, IL-33, and Myc were the three overlapped genes of the DEGs and the necroptosis gene set. Gene set enrichment analysis (GSEA) of Panx1-associated pathways was performed. AC16 cardiomyocytes subjected to OGD/R (simulating MI/RI) were divided into 4 groups: the control group, the OGD/R group, the OGD/R+si-Panx1 group, and the OGD/R+si-Panx1+ dehydrocorydaline (DEH; p38 MAPK agonist) group. Cellular proliferation was assessed by EdU assay, while cell damage was evaluated via lactate dehydrogenase (LDH) release assay. TNF-α, IL-6, and IL-1β levels were measured by ELISA. Western blotting was used to measure the expressions of Panx1, phosphorylated p38 MAPK (p-p38 MAPK), phosphorylated necroptosis markers (receptor-interacting serine/threonine-protein kinase 1［RIPK1］, RIPK3, and mixed lineage kinase domain-like pseudokinase ［MLKL］). Reactive oxygen species (ROS) levels were determined by immunofluorescence, and mitochondrial membrane potential and necroptosis were quantified via flow cytometry. Mitochondrial ultrastructure was examined by transmission electron microscopy. The results showed that GSEA revealed that  Panx1 regulated the p38 MAPK signaling pathway. OGD/R treatment significantly reduced AC16 cell proliferation while increasing LDH release and expressions of Panx1, p-RIPK1, p-RIPK3, p-MLKL, and p-p38 MAPK (P<0.01).   Panx1 knockdown enhanced AC16 cell proliferation, decreased levels of LDH, Panx1, p-RIPK1, p-RIPK3, p-MLKL, p-p38 MAPK, ROS, and necroptosis (P<0.01), ameliorating mitochondrial damage. DEH treatment reversed the protective effects of   Panx1 knockdown. These findings demonstrate that   Panx1 inhibition attenuates OGD/R-induced cardiomyocyte necroptosis, likely through suppression of the p38 MAPK signaling pathway. 
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  The deubiquitinase USP25 supports colonic inflammation and bacterial infection and promotes colorectal cancer

  DUAN Qi, YIN Baochun, LIU Xiaohong

  Current Immunology. 2026, 46(3): 350-357.

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   To investigate the effect of ubiquitin-specific protease 25 (USP25) intervention on macrophage M1 polarization and sepsis-associated acute lung injury (ALI), mouse monocytic macrophages (RAW264.7) were transfected with si-Ctrl or si-USP25 plasmids, then stimulated with LPS to induce M1 polarization. Cells were divided into the control group, the LPS group, the LPS+si-Ctrl group, the LPS+si-USP25 group, and the LPS+si-USP25+PKM2 agonist (DASA-58) group. M1 polarization was assessed by flow cytometry. Co-immunoprecipitation was used to evaluate USP25-PKM2 interaction. Western blotting was used to measure the expression of glycolytic enzymes (PKM2, HK2), M1 macrophage markers (CD86, inducible nitric oxide synthase ［iNOS］), and PKM2 ubiquitination. A cecal ligation and puncture (CLP) sepsis model was established, and mice were divided into the sham group, the CLP group, and the CLP+USP25 inhibitor (AZ1) group. Lung injury was evaluated using H-E staining. TNF-α, IL-1β, and IL-18 levels were quantified by ELISA. CD86+ M1 macrophages were detected by immunofluorescence. The results showed that, compared to the LPS group, the LPS+si-USP25 group showed reduced M1 macrophage polarization ratio, decreased protein expression levels of PKM2, HK2, CD86, and iNOS, and increased PKM2 ubiquitination (P<0.01). In contrast, the LPS+si-USP25+DASA-58 group exhibited elevated M1 polarization ratio, CD86, and iNOS expression compared to those of the LPS+si-USP25 group (P<0.01). Relative to the sham group, CLP mice demonstrated aggravated pulmonary inflammatory injury, heightened levels of TNF-α, IL-1β, and IL-18, increased M1 macrophage infiltration, as well as elevated PKM2, HK2, CD86, and iNOS expressions (P<0.01). Compared to those of the CLP group, the pathological damage of lung tissue, inflammatory factors, the proportion of M1 type polarization of macrophages, and the protein expression levels of PKM2, HK2, CD86, and iNOS in the CLP + AZ1 group were all decreased (P<0.01).  Taken together, this study confirms that inhibiting USP25 can block macrophage glycolysis and M1 polarization to alleviate sepsis-induced lung injury, with a mechanism involving the induction of PKM2 ubiquitination to reduce its protein expression level.
  

  
  
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  IRF-1 mediates inflammasome activation to regulate microglial pyroptosis and Aβ phagocytosis

  ZOU Zhengshou, PEI Pei

  Current Immunology. 2026, 46(3): 358-365.

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  Abstract：  This study aims to investigate the effects of interferon regulatory factor 1 (IRF-1) on pyroptosis and inflammasome activation in BV2 microglial cells, as well as its impact on BV2 cell phagocytosis of amyloid β-protein (Aβ). A single-cell brain dataset was used to screen for the differentially expressed gene IRF-1 in brain tissues of Alzheimer's disease (AD) patients and normal controls, analyze its expression across various cell types, and perform functional enrichment analysis. BV2 cells were stimulated with Aβ1-42 to mimic the inflammatory environment of AD and were divided into the control group, the model group (treated with Aβ1-42), the Aβ1-42+sh-NC group, the Aβ1-42+sh-IRF-1 group, and the Aβ1-42+sh-IRF-1+ML385 (Nrf2 inhibitor) group. Cell viability was assessed using the CCK-8 assay. Pyroptosis levels were evaluated using lactate dehydrogenase (LDH) release assay and Annexin V-FITC/PI double staining. Western blotting was performed to detect the expression levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), Caspase-1, Gasdermin D N-terminal domain (GSDMD-N), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). ELISA was used to measure the levels of IL-1β and IL-18. Reactive oxygen species (ROS) levels in BV2 cells were detected using DCFH-DA fluorescence staining. The phagocytic capacity of BV2 cells for Aβ was assessed using flow cytometry. Compared with the control group, the model group showed decreased BV2 cell viability, increased expressions of inflammasome-related molecules, including NLRP3, ASC, Caspase-1, and GSDMD-N, elevated levels of IL-1β, IL-18, LDH release, and pyroptosis rate, increased intracellular ROS production, and decreased protein expressions of Nrf2 and HO-1 (P<0.01). Compared with the model group, the Aβ1-42+sh-IRF-1 group exhibited significantly increased cell viability and Aβ phagocytic capacity, decreased levels of IL-1β and IL-18, downregulated expression of inflammasome and pyroptosis-related proteins, reduced LDH release, pyroptosis rate, and ROS production, as well as increased protein expressions of Nrf2 and HO-1 (P<0.01). Compared to those of the Aβ1-42+sh-IRF-1 group, BV2 cell pyroptosis levels were reversed in the Aβ1-42+sh-IRF-1+ML385 group. The results suggest that intervening IRF-1 reduces NLRP3 inflammasome activation and pyroptosis in Aβ1-42-induced BV2 cells, and the mechanism may involve activation of the Nrf2/HO-1 signaling pathway.
  

  
  
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  FBXL18 knockdown inhibits the immune evasion of colon cancer cells via regulating PD-L1 ubiquitination

  ZHANG Yunjie, LIU Jien, LI Minghui, GUO Minghai, ZHANG Wulin, SONG Xuebing

  Current Immunology. 2026, 46(3): 366-375.

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  This study investigates the inhibitory effect of F-box and leucine-rich repeat protein 18 (FBXL18) knockdown on immune evasion of colon cancer by regulating the ubiquitination of PD-L1. Colon cancer cell line CT26 was transfected with sh-NC or sh-FBXL18 plasmids or infected with empty (NC-OE) or FBXL18 overexpression (FBXL18-OE) lentivirus vectors. CCK-8 and colony formation assays were used to measure CT26 cell proliferation and clonogenic ability. A subcutaneous tumor model was established in Balb/c mice using CT26 cells, and the mice were divided into the model group, the sh-NC group, and the sh-FBXL18 group. Flow cytometry was used to determine the proportion of CD8+ T cells in tumor tissue. Immunofluorescence staining was used to assess the infiltration of the CD8+ T subset Tc1 cells in tumor tissue. ELISA was used to measure levels of perforin, granzyme and TNF-α in tumor tissue. CT26 cells were co-cultured with CD8+ T cells and divided into the control group (CT26 cells alone), the model group (CT26 co-cultured with CD8+ T cells), the sh-NC /NC-OE group (CT26 transfected with sh-NC or infected with empty vector lentivirus, then co-cultured with CD8+ T cells), and the sh-FBXL18/FBXL18-OE group (CT26 transfected with sh-FBXL18 or overexpressing FBXL18, then co-cultured with CD8+ T cells). ELISA was used to measure lactate dehydrogenase (LDH) level in the supernatant. Western blotting and immunohistochemistry was used to test PD-L1 expression in tumor tissue. Co-immunoprecipitation and immunofluorescence staining confirmed the interaction and co-localization of PD-L1 and FBXL18 in CT26 cells. The results showed that compared to the control group, sh-FBXL18 CT26 cells showed reduced PD-L1 expression (P<0.01) and increased ubiquitination levels. Compared to the model group, the sh-FBXL18 group exhibited slower tumor growth, increased proportions of CD8+ T and Tc1 cell infiltration in tumor tissue, elevated levels of perforin, granzyme, and TNF-α (P<0.01), and reduced PD-L1 (P<0.01). In the co-culture experiments, knocking down FBXL18 in CT26 cells enhanced T cell-mediated killing of cancer cells (P<0.05), increased perforin, granzyme, and TNF-α levels (P<0.01), while overexpressing FBXL18 suppressed T cell cytotoxicity (P<0.01). FBXL18 and PD-L1 were found to directly interact and co-localize in CT26 cells. This study suggests that knocking down FBXL18 promotes the cytotoxic function of CD8+ T cells against colon cancer cells, and the mechanism involves promoting the ubiquitination of PD-L1 in colon cancer cells.
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  Exosome from si-CCL3 transfected BMSC ameliorates lung injury in septic mice

  LUO Hui, XU Yi

  Current Immunology. 2026, 46(3): 376-385.

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  To investigate whether small interfering RNA (siRNA) mediated knock down of C-C motif chemokine ligand 3 (CCL3) expression  can inhibit lung injury in septic mice by secreting exosomes, a septic mouse model was established using cecal ligation and puncture (CLP). H-E staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining were used to validate the septic mouse model. The expression of CCL3 in the lung tissue of septic mice was detected using immunohistochemistry, immunofluorescence staining, and qRT-PCR. Three CCL3 silencing plasmids (si-CCL3 1#, si-CCL3 2#, and si-CCL3 3#) were constructed using siRNA technology and transfected into bone marrow mesenchymal stromal cells (BMSC). The optimal transfection plasmid was screened by qRT-PCR. Exosomes were extracted from the supernatant and validated using transmission electron microscopy and Western blotting. The phagocytosis of PKH26-labeled exosomes by alveolar epithelial cells (MLE-12) was observed using confocal microscopy. Cell proliferation was assessed using the CCK-8 assay, and the expressions of IL-1β and IL-6 in the supernatant were measured using ELISA. Mice were divided into 3 groups: the control group, the model group, and the exosome group. H-E staining, TUNEL staining, and PAS staining were used to validate the reparative effects of exosomes secreted by BMSC transfected with si-CCL3 silencing plasmids on lung injury in septic mice. The results showed that CCL3 level in the lung tissue of the septic group was significantly increased (P<0.01), while the si-CCL3 3# plasmid reduced the relative expression of CCL3 mRNA. After MLE-12 cells pretreated with H2O2 phagocytosed exosomes derived from si-CCL3 3# transfected BMSC, the cell proliferation rate increased, and the expression levels of inflammatory factors (IL-1β and IL-6) were significantly reduced (P<0.05). H-E staining, TUNEL staining, PAS staining, and immunohistochemical staining results demonstrated that exosomes derived from si-CCL3 transfected BMSC could inhibit the inflammatory response in the lung tissue of septic mice. The TUNEL-positive cell rate in the lung tissue was significantly reduced, the levels of mucus and glycoproteins in the lung tissue were significantly decreased, and the expression of IL-6 was significantly reduced (P<0.05). In summary, exosomes derived from si-CCL3 transfected BMSC can inhibit lung injury in septic mice.
  

  
  
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  Factors regulating the inhibitory effect of mesenchymal stem cells on peripheral blood mononuclear cell proliferation

  LIAO Xia, WU Jianfu, LUO Zhiyong, WANG Dan, DAI Xicheng, TANG Kai, PAN Xinghua, ZHANG Fen, LIANG Xiao

  Current Immunology. 2026, 46(3): 386-393.

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  To systematically explore the regulatory factors of mesenchymal stem cells (MSC) on the proliferation inhibition of PBMC, and establish a standardized evaluation system， the 4th-generation umbilical cord MSC were used for cell morphology, cell surface marker, and trilineage differentiation identification. MSC were co-cultured with PHA-P-induced PBMC in direct contact. The proliferation inhibition rate was detected by CFSE labeling combined with flow cytometry. The effects of PBMC source, MSC∶PBMC ratio, stimulant concentration, culture time, and MSC pretreatment were analyzed. The MSC used in the experiment met the requirements of standard MSC confirmed by morphology, cell surface markers, and trilineage differentiation identification. The proliferation inhibition rate of PBMC by MSC decreased with the reduction of the MSC∶PBMC ratio in a dose-dependent manner. The inhibition rate of single-source PBMC was higher than that of mixed-source PBMC, suggesting that the interaction between allogeneic cells might interfere with the results. The proliferation increased with time and stimulant concentration, requiring a balance within an appropriate range to highlight the inhibitory effect of MSC. IFN-γ induction enhanced the inhibitory ability of MSC, indicating that cell pretreatment may optimize the detection method. The proliferation inhibition effect of MSC on PBMC was affected by PBMC source, MSC type, MSC∶PBMC ratio, PHA-P concentration, and co-culture time. By evaluating the influence of various factors on MSC-mediated PBMC proliferation inhibition, this study summarizes multi-dimensional experimental data and provides an experimental basis for the quality evaluation of MSC immunomodulatory function.
  

  
  
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  Research progress on signal protein Pin1 in autoimmune diseases

  ZHANG Yuxia, LIANG Liuna, CHEN Ying, ZHOU Shuhong

  Current Immunology. 2026, 46(3): 394-399.

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  Peptidyl-prolyl cis/trans isomerase never in mitosis A(NIMA)-interacting 1 (Pin1) regulates the phosphorylation level and biological activity of various proteins as well as multiple signaling pathways by isomerization which may participate in disease occurrence and development. Therefore, exploring the regulatory role of Pin1 in signaling pathways related to autoimmune diseases and the underlying mechanism may provide new ideas and targets for the treatment of immune diseases.
  

  
  
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  Research progress on HLA-G in colorectal cancer

  HAN Qiuyue, CHEN Qiongyuan, LIN Aifen

  Current Immunology. 2026, 46(3): 400-405.

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  HLA-G is a non-classical MHC class Ⅰ molecule initially discovered to be expressed in the trophoblast cells at the maternal-fetal interface, and was  reported as an immune tolerance molecule. In recent years, HLA-G has garnered significant attention for its role as a novel immune checkpoint  molecule in the tumor immune microenvironment. HLA-G binds to immune cells expressing immunoglobulin-like transcript (ILT)-2 and ILT-4. The HLA-G/ILT-2/4 (HLA-G/ILT) signaling pathway promotes immunosuppression, leading to tumor immune evasion. Several tumor immunotherapies targeting HLA-G have entered clinical trials, providing new strategies for the immunotherapy of solid tumors such as colorectal cancer. This review aims to explore and summarize the role of HLA-G in the immune microenvironment of colorectal cancer, reveal the potential mechanisms by which HLA-G regulates the immune microenvironment of colorectal cancer, and provide a theoretical basis for targeting HLA-G in conjunction with immune checkpoint therapy for colorectal cancer.
  

  
  
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  ILC2 metabolic immunoregulation: a new perspective on the diagnosis and treatment of cardiovascular diseases

  WU Meng, WANG Yu

  Current Immunology. 2026, 46(3): 406-411.

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  Cardiovascular disease (CVD) is a major global health challenge, and its residual inflammation and fibrosis constitute the main bottleneck of current therapy. ILC2, as a crucial hub linking innate immunity and metabolic homeostasis, shows great potential in diagnosis and treatment. This review systematically elaborates on the dual regulatory role of ILC2 in CVD. ILC2 secrets IL-4, IL-5, IL-13, amphiregulin (AREG) and bone morphogenetic protein 7 (BMP-7) to stabilize plaques in atherosclerosis (AS) by promoting M2 macrophage polarization and neutralizing oxidized low density lipoprotein (oxLDL). In addition, they drive the “ILC2-eosinophil-macrophage” repair axis to suppress adverse remodeling after myocardial infarction (MI). However, under chronic metabolic disorders (such as obesity), the liver kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) axis is impaired, which can lead to enhanced mitophagy in ILC2, overexpression of PD-1 and functional exhaustion, while  disrupting the “neuronal-mesenchymal-ILC2” regulatory network. This intensifies inflammation and insulin resistance, accelerates CVD progression, and under certain conditions ILC2 can even participate in pro-fibrotic processes. A deep understanding of the plasticity of ILC2 function provides new directions for targeted intervention, such as targeting ILC2 metabolic checkpoints (e.g. PD-1 blockade), using IL-33 to expand activated ILC2, and applying BMP-7 derived peptides. These strategies are expected to open new avenues for overcoming the current therapeutic dilemma of CVD.
  

  
  
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  Research progress on the relationship between calcium-activated chloride channel TMEM16A and inflammatory responses

  QU Chao, PENG Jiawei, QIU Yunting, LI Hongyan, ZHAO Entong, GUAN Xin

  Current Immunology. 2026, 46(3): 412-416.

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  The calcium-activated chloride channel (CaCC) TMEM16A is an important ion channel protein that is widely involved in physiological and pathological processes, including epithelial cell mucus secretion, cell proliferation, and inflammatory responses. In recent years, with the deepening research into inflammation mechanisms, increasing evidence has shown that various inflammatory factors, including IL-4, IL-13, IL-6, and IL-8, significantly promote the expression of TMEM16A and participate in its functional regulation. Meanwhile, TMEM16A itself can act as a key regulatory factor in inflammatory signaling pathways, playing an important role in the development of respiratory inflammation, intestinal epithelial barrier dysfunction, cancer and chronic rhinosinusitis with nasal polyps, by activating various inflammatory signaling pathways including the inositol 1,4,5-trisphosphate receptor (IP3R)-mediated calcium signaling pathway, the NF-κB signaling pathway, and the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Notably, depending on the severity of the disease, the state of cell proliferation, and the interactions among different components, TMEM16A exerts distinct pathological roles in different inflammatory diseases. This review summarizes the relationship between TMEM16A and inflammatory responses, and discusses its potential as a therapeutic target.