30 July 2025, Volume 45 Issue 4

    

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  Correlation between HAX-1 and disease activity of lupus nephritis

  ZHAO Jingjing, CHEN Haojie, WANG Wenwen, GAO Yingying

  Current Immunology. 2025, 45(4): 381-389.

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  To investigate the role of HS1-associated protein X-1 (HAX-1) in lupus nephritis (LN) patients, 50 patients with SLE were selected as the study objects, and 29 healthy patients were selected as the control group. qRT-PCR was used to detect the mRNA expression of HAX-1  in PBMC. The expression of HAX-1 in kidney tissue was detected by immunohistochemistry (IHC). The proportions of CD4⁺ CD25⁺ Foxp3⁺ Treg and CD4⁺ IL-17A⁺ Th17 in peripheral blood were measured by flow cytometry. Human renal mesangial cells (HRMC) were cultured in vitro, and HAX-1 silencing plasmid and HAX-1 overexpression plasmid were transfected. Flow cytometry and MTT were used to measure the apoptosis and proliferation of HRMC after transfection, respectively. Western blotting was used to detect the expressions of proliferation-related signal PI3K/Akt and apoptosis-related signal Bax/Casepase-9. The results showed that the mRNA expression level of HAX-1  in PBMC of the active LN group was significantly higher than that of the NRA-SLE group (P<0.001). Meanwhile, HAX-1  mRNA  expression level was positively correlated with SLE disease activity index (SLEDAI-2K) and 24 h urinary protein quantity in peripheral blood (R2= 0.876, P<0.001; R2=0.409, P<0.001). The IHC results showed that the expression level of renal HAX-1 in the active LN group was significantly higher than that of the normal control group (P<0.001). The expression level of HAX-1 in renal tissue was positively correlated with LN activity score and chronicity score (r=0.975, P<0.001; r=0.667, P=0.002). Overexpression of HAX-1 reduced apoptosis (P<0.001) and increased the proliferation activity of HRMC (P<0.001). Meanwhile, the levels of PI3K and p-Akt significantly increased (P<0.001) while the levels of Bax/Casepase-9 significantly decreased (P<0.001). In contrast, upon transfection of HAX-1 silencing plasmid, the apoptosis of HRMC was significantly increased (P<0.001), and the proliferation activity was significantly reduced (P<0.001), along with significantly reduced PI3K and p-Akt expression (P<0.001), increased Bax/Casepase-9 expression(P<0.001). These results suggest that HAX-1 expression in peripheral blood and kidney tissues of patients with active LN group is closely related to kidney involvement and disease activity, as well as the imbalance of the CD4⁺ IL-17A⁺ Th17 and CD4⁺ CD25⁺ Foxp3⁺ Treg. Using a system of HRMC cultured in vitro, this study demonstrates that HAX-1 can promote the pathogenesis  of glomerular nephritis in LN by affecting the signaling pathways related to mesangial cell proliferation and apoptosis. HAX-1 may have a dual effect on Th17/Treg balance and HRMC proliferation, contributing to the pathogenesis of LN. 
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  Effects of Bupiqiangli compound on Th17/Treg differentiation of thymic lymphocytes in myasthenia gravis rats

  WANG Qiang, LI Ruozhao, LOU Jinbo, KUANG Shixiang, QIAN Yijia, YONG Bo, GUO Jing, LIU Yunquan

  Current Immunology. 2025, 45(4): 390-396.

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  This study aimed to investigate the effect of Bupiqiangli compound on Th17/Treg differentiation of thymic lymphocytes in rats with myasthenia gravis. CCK-8 was used to determine an optimal 10% serum concentration for subsequent experiments. Cells were divided into 8 groups: the normal group (control), the normal+blank serum group (control+BS), the myasthenia gravis model group (model), the myasthenia gravis model+blank serum group (model+BS), the myasthenia gravis model+low-dose Bupiqiangli compound treatment serum group (model+LBPQL), the myasthenia gravis model+medium-dose Bupiqiangli compound treatment serum group (model+MBPQL), the myasthenia gravis model+high-dose Bupiqiangli compound treatment serum group (model+HBPQL), and the myasthenia gravis model+prednisone containing serum group (model+prednisone). After treated with serum for 24 hours, the proportions of Th17 and Treg cells in each group were detected by flow cytometry. ELISA was used to detect the content of IL-17 and TGF-β in the supernatant. Western blotting was used to measure the protein levels of Notch1, Hes1, Hes5 and Hey1. The results showed that, compared to that of the spleen deficiency model group, the proportion of Th17 cells in the model+HBPQL group and the model+Prednisone group decreased significantly (P<0.05), while the proportion of Treg cells increased significantly (P<0.05). The expression of IL-17 was significantly decreased (P<0.05), while the expression of TGF-β was significantly increased (P<0.05). The protein expressions of Notch1, Hes1, Hes5, and Hey1 were significantly decreased (P<0.05). The results indicate that Bupiqiangli compound can regulate the proportions of Th17 and Treg in thymic lymphocytes in rats with myasthenia gravis. The underlying mechanism may involve the regulation of the Notch signaling pathway. 
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  Performance verification of time-resolved fluorescence immunoassay on human serum anti-phospholipase A2 receptor antibody IgG4

  LIN Huisong, ZHENG Tianyu, WANG Binrong, JIANG Xiaolu, LI Yong, HUANG Biao

  Current Immunology. 2025, 45(4): 397-401.

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  The objective of this study was to verify the performance of time-resolved fluorescence immunoassay for human serum anti-phospholipase A2 receptor antibody IgG4 (PLA2R-IgG4) including the linear range, accuracy, precision, specificity, and performance of PLA2R-IgG4 reagent with magnetic particle time-resolved fluorescence immunoassay. The results showed that the blank limitation was 7.02 ng/mL, linear range was 50.00 ng/mL-10 000.0 ng/mL, accuracy was 86.28%-104.58%, intra-batch precision was 2.62%-5.33%, inter-batch precision was 7.37%-8.26%, and the specificity was in acceptable range. The detection rate of PLA2R-IgG4 in 77 idiopathic membranous nephropathy patients was 75.32%, and the test results of 15 patients with secondary membranous nephropathy were all negative. All the indexes of this method meet the requirements of clinical test quality, and this method shows a better detection rate for idiopathic membranous nephropathy, making it promising in clinical translation. 
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  The protective effect of miR-34b-5p on sepsis induced acute lung injury in rats through the PTEN/Akt/mTOR pathway

  ZHANG Hongyu, LI Xin, WU Qinfen, LONG Xiaoyan

  Current Immunology. 2025, 45(4): 402-408.

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  To explore the protective effect of miR-34b-5p on sepsis induced acute lung injury (ALI) in rats and its impact on the phosphatase and tensin homolog (PTEN)/Akt/mTOR pathway, 80 specific pathogen free grade male SD rats were randomly divided into the sham group, the model group, the empty vector group, and the miR-34b-5p group, with 20 rats in each group. The rats in the sham group only underwent laparotomy, while the remaining rats were subjected to cecal ligation and perforation to establish a sepsis model. After the establishment of the model, rats in the empty vector group and the miR-34b-5p group were injected with empty vectors and miR-34b-5p overexpression plasmids through the tail vein, respectively. Rats in the model group and the sham group were injected with equal amount of physiological saline. Three days after injection, ELISA was used to determine the IL-1β and IL-6 levels in rat peripheral blood. The wet weight/dry weight  (W/D）ratio of rat lung tissue was calculated and the pathological changes of rat lung tissue was observed by H-E staining. The apoptosis of lung histiocyte cells was detected by TUNEL method. miR-34b-5p, IL-1β and IL-6 mRNA levels in lung tissue were detected by qRT-PCR. Western blotting was used to detect the protein levels of PTEN, p-Akt, p-mTOR, Akt, mTOR, B cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and Caspase-3. The results showed that the alveoli in the sham group appeared normal, while those of the model group and the empty vector group were collapsed, along with thickened alveolar walls, vascular congestion, pulmonary interstitial congestion, edema, and inflammatory cell infiltration. The infiltration of inflammatory cells in the lung tissue of rats in the miR-34b-5p group was reduced, and alveolar injury was significantly improved. Compared to those of the sham group, the expressions of IL-1β and IL-6 at both protein and mRNA levels, the number of apoptotic cells, levels of Bax, Caspase-3 and PTEN as well as W/D ratio were significantly increased in the model group (P<0.01), while the levels of miR-34b-5p, Bcl-2 protein, p-Akt/Akt ratio, and p-mTOR/mTOR ratio were significantly decreased (P<0.01). Compared to those of the empty vector group, the miR-34b-5p expression, Bcl-2 protein level, p-Akt/Akt and p-mTOR/mTOR ratio in the lung tissue of the miR-34b-5p group were significantly increased (P<0.01), while the IL-6, IL-1β protein and mRNA levels, the number of apoptotic cells, the Bax, PTEN, Caspase-3 protein levels, and W/D ratio were significantly decreased (P<0.01). This study suggests that miR-34b-5p alleviates pulmonary inflammation and cell apoptosis of ALI in sepsis rats through the PTEN/Akt/mTOR pathway.
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  Efficiency analysis of a fully automated ultra immunoassay system based on high-throughput flow fluorescence technology for detecting autoantibodies

  WANG Haixia, FENG Yangfan, CHEN Qing, DU Weipeng, LIANG Jingyi, LI Jiawei, ZHAO Yingying

  Current Immunology. 2025, 45(4): 409-414.

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  This study aimed to evaluate the performance and property of a fully automated ultra-high speed immunoassay system based on high-throughput flow fluorescence technology for detecting autoimmune antibodies in clinical laboratories. According to the laboratory accreditation guidelines issued and implemented by the China National Accreditation Commission for Conformity Assessment (CNAS), flow fluorescence technology was used to detect the autoantibodies and evaluations  were made on parameters including the precision, linear range, accuracy, and limit of blank (LOB). When conducting repeatability validation on quality control products at both low and high concentrations, the average standard deviation and coefficient of variation (CV)  were calculated of each antibody level in the 16 antibody profiles. The CV of all antibodies were lower than 7% and 5%, respectively, which were within the less than 10% range as declared by the manufacturer. The first-order polynomial linear regression coefficients for resistance to anti-C1q-Ab and resistance to anti-dsDNA-Ab were 0.999 and 0.996, respectively, with correlation coefficient  above 0.999. The deviation distributions were all within 3% and the results of the 2 recovery experiments were 91.56% and 105.60%, respectively. When Oumeng company imprinting method was used as a reference, the compliance rates of the validation projects were all above 92%. Values of LoB for anti-C1q-Ab and anti-dsDNA-Ab were both within 0.5 U/ml and 3 IU/ml, respectively. In conclusion, all performance parameters of the flow cytometry fluorescence technology for autoantibody detection are consistent with the manufacturer's specifications and pass the standard of clinical requirements. It can replace similar imported instruments.
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  IL-36 signaling pathway regulates monocytes function in patients with B-cell acute lymphoblastic leukemia

  SUN Xi, WANG Wenhuan

  Current Immunology. 2025, 45(4): 415-421.

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  The study aims to elucidate the mechanism by which IL-36 regulates monocytes in the pathogenesis of acute B-cell lymphoblastic leukemia (B-ALL). Forty-seven B-ALL patients and 20 controls were enrolled. Serum from patients and controls was collected and PBMCs were isolated. Monocytes and CD4⁺ T cells were purified. ELISA was used to measure and compare the serum IL-36α, IL-36β, IL-36γ, and IL-36 receptor antagonist (IL-36RA) levels between the 2 groups. mRNA levels of IL-36 receptors in monocytes were compared using qRT-PCR. Monocytes were stimulated with recombinant IL-36β or IL-36γ and cell proliferation, granzyme A secretion, granzyme B, granzyme H, IFN-γ, IL-1β, and IL-6 were compared before and after stimulation. mRNA levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), Fas ligand (FasL), PD-1 and CTLA-4 expressions in monocytes were also compared. IL-36β- and IL-36γ-stimulated monocytes were co-cultured with autologous CD4⁺ T cells and the Th1 and Th17 percentages were compared. The results showed that, compared to those of controls, the IL-36β and IL-36γ levels were significantly lower in B-ALL patients （P<0.001）. There were no statistical differences of serum mRNA levels of IL-36α/IL-36RA or IL-36 receptor between groups (P>0.05). There were also no significant difference in cellular proliferation, IFN-γ secretion, TRAIL/FasL mRNA, or CTLA-4 expression in monocytes upon stimulation with IL-36β or IL-36γ (P>0.05). The IL-1β and IL-6 secretion increased (P<0.05) while PD-1 expression decreased (P<0.001) compared to those of the unstimulated group. Granzyme A, granzyme B, and granzyme H levels were significantly higher only upon IL-36γ stimulation (P<0.05). There was no significant difference in the percentages of Th1 or Th17 (P>0.05) in the co-culture system of IL-36β or IL-36γ stimulated monocytes and CD4⁺ T cells. This study suggests that IL-36β and IL-36γ levels are down-regulated in B-ALL patients, which might impair the killing activity of monocytes and promote B-ALL progression.
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  Mechanical study of GSTM3 regulated renal tubular epithelial cell pyroptosis in renal inflammatory response in hyperuricemia

  ZHANG Yu, GAO Bo, QIAN Hao

  Current Immunology. 2025, 45(4): 422-430.

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  This study aims to investigate the regulatory effect of glutathione S-transferase mu 3 (GSTM3) on renal tubular epithelial cells HK-2 pyroptosis and renal inflammation in hyperuricemia (HUA). GSE186871 data set was used to screen for kidney differentially expressed genes in HUA and normal mice. The mice were divided into the normal group, the model group, the normal + adenovirus shRNA (normal + Ad-sh-NC) group, the model+Ad-sh-NC group (Ad-sh-NC group), and adenovirus GSTM3 shRNA group (Ad-sh-GSTM3 group）. HK-2 cells were divided into the control group, the model group, the control + Ad-sh-NC group, the Ad-sh-NC group, and the Ad-sh-GSTM3 group. Cell survival rate was measured by CCK-8 method. Renal pathology was observed by H-E staining. The levels of serum uric acid (UA), creatinine (Cr)，and blood urea nitrogen (BUN) were detected by a biochemical analyzer. IL-1β and IL-18 levels were detected by ELISA. Western blotting was used to detect GSTM3, Caspase-1, NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), gasdermin D (GSDMD)-N, and Cleaved GSDMD-N expressions. The expressions of GSTM3 and GSDMD-N in kidney were detected by immunohistochemistry. The results showed that compared to the normal group, the model group showed renal tubule swelling and local inflammatory cell infiltration. The expressions of GSTM3, Caspase-1, NLRP3, GSDMD-N, and Cleaved GSDMD-N in renal tissue, and serum levels of Cr, BUN, UA, IL-1β, and IL-18 were all increased (P<0.05). Compared to the model group, the Ad-sh-GSTM3 group exhibited reduced renal tubule injury, decreased levels of Cr, BUN, UA, IL-1β, and IL-18 (P<0.01), and decreased protein expressions of GSTM3, Caspase-1, NLRP3, GSDMD-N, and Cleaved GSDMD-N (P<0.05). Compared to those of the control group, the HK-2 cell survival rate in the model group was decreased (P<0.01), along with increased IL-1β and IL-18 levels in the supernatant (P<0.01), and increased protein expressions of GSTM3, Caspase-1, NLRP3, GSDMD-N, and Cleaved GSDMD-N (P<0.01). Compared to the model group, the Ad-sh-GSTM3 group showed increased HK-2 cell survival rate (P<0.01), decreased IL-1β and IL-18 levels (P<0.01), and decreased protein expressions of GSTM3, Caspase-1, NLRP3, GSDMD-N, and Cleaved GSDMD-N (P<0.01). Therefore, inhibition of GSTM3 effectively inhibits the pyroptosis of renal tubular epithelial cells and alleviate the renal inflammatory injury caused by HUA.
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  IL-27 regulates multiple myeloma progression by inducing Th17/Treg imbalance

  YE Xizhong

  Current Immunology. 2025, 45(4): 431-438.

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  The study aims to investigate the effect of IL-27 on multiple myeloma (MM) via the imbalance of Th17 and Treg. Peripheral blood samples from 10 MM patients and 10 healthy individuals were collected. qRT-PCR was used to detect IL-27, Th17-related factors (retinoic acid receptor-related orphan receptor gamma t ［RORγt］, IL-17A, and IL-6) and Treg-related factors (IL-10 and forkhead box protein 3 ［Foxp3］) in the peripheral blood. Western blotting was used to detect the key transcriptional pro-factors of Th17 and Treg. Flow cytometry was used to detect the changes in the ratios of Th17 and Treg in peripheral blood, and qRT-PCR was used to detect the cytokines secreted by Th17 (RORγt, IL-17A, IL-21, and IL-22) and the anti-inflammatory factors (Foxp3, IL-10, IL-35, and TGF-β) secreted by Treg in PBMC. RPMI-8226 cells were used to construct oe-NC/oe-IL-27 and si-NC/si-IL-27 cell lines. ELISA was used to detect the level of IL-27 in the supernatant of myeloma cells. Flow cytometry was used to detect the proportion of Th17 co-cultivated with CD4⁺ T cells in the overexpression cells. CCK-8 and Transwell assays were used to detect the cell viability, migration and invasion ability. The results showed that the levels of IL-27 and Treg-related factors (IL-10 and Foxp3) were increased (P<0.05) and Th17-related factors (RORγt, IL-17A, and IL-6) were decreased in the MM group (P<0.05). There was no difference in the proportion of Th17 between MM group and normal control group, while the proportion of Treg was increased in MM group. Levels of cytokines secreted by Th17 (RORγt, IL-17A, IL-21, and IL-22) were decreased (P<0.05) and anti-inflammatory factors secreted by Treg (Foxp3, IL-10, IL-35, and TGF-β) were increased in PBMC of MM patients (P<0.05). Myeloma cells could secrete IL-27. Th17-related factors (RORγt, IL-17A, IL-21, and IL-22) in the oe-IL-27 group decreased (P<0.05) while the cell viability increased (P<0.05). The above results of the oe-IL-27 group were reversed in the si-IL-27 group. This preliminary study confirms that IL-27 promotes MM progression via Th17/Treg imbalance.
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  Diagnostic and regulatory functions of KIF11 in lung adenocarcinoma

  LI Xin

  Current Immunology. 2025, 45(4): 439-447.

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  To investigate the diagnostic value and biological functions of kinesin family member 11 (KIF11) in lung adenocarcinoma (LUAD) patients, this study utilized bioinformatics platforms and statistics (The Cancer Genome Atlas ［TCGA］, Human Protein Atlas ［HPA］, and ROC curve) to examine the expression of KIF11 in LUAD tissues and its relationship with patient survival, as well as the association between KIF11 and the clinicopathological features. Pearson correlation analysis was used to study the association between KIF11 expression and the 22 types of immune cells infiltration. qRT-PCR was used to detect the relative mRNA expression of KIF11 in LUAD cell lines. Western blotting was used to detect the expressions of KIF11 protein, epithelial-mesenchymal transition (EMT)-related proteins, and of cell cycle-related proteins. CCK8 assay, colony formation assay, Transwell assay, scratch healing assay, and flow cytometry were used to detect tumor cell proliferation, migration and invasion abilities, as well as cell cycle distribution, respectively. The results showed that KIF11 and  its protein were highly expressed in LUAD tissues and cell lines (all with P＜0.05), KIF11 level was closely connected with the patients clinical characteristics (all with P＜0.05), and the high expression of KIF11 led to reduced survival rate in patients (P＜0.05). Pearson correlation analysis revealed that the expression of KIF11 was positively correlated with the infiltration of the majority of immune cells (all with r＞0). Down-regulation of KIF11 expression inhibited the proliferation (P＜0.01), migration (P＜0.000 1) and invasion abilities (P＜0.01) of LUAD cells, increased the proportion of G2/M phase cells (P＜0.001), decreased the proportion of G0/G1 phase cells (P＜0.001), promoted apoptosis (P＜0.000 1), and inhibited the EMT process  (all with P＜0.05). This study demonstrates that KIF11 may be used as a diagnostic marker for LUAD, and down-regulation of the expression of KIF11 inhibits LUAD tumor cell progressive phenotypes.
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  Distribution of PD-1 on peripheral blood T cells in  colon cancer patients with different stages  and its connection with immunotherapy efficacy

  XU Zhonghai, LYU Yaodou, ZHANG Zhanjiao, LI Xiaojun, LIU Guangyao

  Current Immunology. 2025, 45(4): 448-456.

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  The study aims to investigate the expression level of PD-1 on peripheral blood T cells among colon cancer patients with different stages and its connection with immunotherapy efficacy. One hundred and twelve colon cancer patients were enrolled in to analyze the relationship between PD-1 expression and clinical parameters. Based on the outcome of immunotherapy, the patients were divided into the effective group (n=85) and the ineffective group (n=27). Multivariate logistic regression formula was used to analyze the relationship between PD-1 expression and clinical characteristics and to screen the factors affecting the efficacy of immunotherapy in the objects. The results showed that there existed statistically significant differences in PD-1 expression among different clinical stages, and among different expression levels of carcinoembryonic antigen (CEA) or carbohydrate antigen 199 (CA199) (all with P＜0.05). However, the results of multivariate logistic analysis showed that the positive expression rate of PD-1 could not be used as an independent predictor for clinical staging (P＞0.05); Low/middle-low differentiation, clinical stage ⅢⅣ, lymph node metastasis, distant metastasis, neutrophil-to-lymphocyte ratio (NLR)≥5, platelet-to-lymphocyte ratio (PLR)≥135, and positive expression of PD-1 all were risk factors predicting ineffective immunotherapy in colon cancer patients (all with P＜0.05). This study suggests that the expression of PD-1 on CD4+T cells in peripheral blood is significantly associated with clinical stages and the efficacy of immunotherapy in colon cancer patients. However, it can not be used as an independent predictor for clinical staging. Meanwhile, PD-1 is sufficient to be used as a biological index for predicting the efficacy of immunotherapy.
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  Research progress on the diagnostic and therapeutic targets of B cells in primary membranous nephropathy

  CHEN Minghui, LIN Jinpiao, SHENG Huiming

  Current Immunology. 2025, 45(4): 457-462.

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  Primary membranous nephropathy (PMN), an autoimmune disease targeting the kidney, is one of the most common causes of nephrotic syndrome in adults. Although clinical treatments have advanced from supportive care to B cell-targeted therapies including rituximab, challenges such as recurrent delays and significant variability in patient prognoses remain pressing issues. This review discusses the pathogenic mechanisms of auto-reactive B cells in PMN, traces the history of autoantigen discoveries, and provides an update on current B cell-targeted treatments, aiming to offer valuable insights for future research.
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  Research progress on the role of glycosylation in inflammatory bowel disease pathogenesis

  FAN Zhenzhen, ZHANG Tiantian, ZHOU He, HOU Linqian, WU Tong, ZHANG Jiaqi, LIU Xiaoning, LIANG Jie

  Current Immunology. 2025, 45(4): 463-468.

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  Inflammatory bowel disease (IBD) is a complex immune disorder of the intestines characterized by chronic inflammation. It primarily includes Crohn's disease (CD) and ulcerative colitis (UC). The study of glycosylation, a common post-translational modification of proteins, is at the forefront of immunology and glycobiology. Recent researches indicate the link between glycosylation and the development of IBD, making it a hot topic in IBD research. However, studies in this area are limited in China. This article provides an overview of glycosylation and its role in IBD, aiming to lay the groundwork for Chinese researchers who are dedicated to the study of glycosylation of IBD and for the translational application of clinical diagnosis and treatment of IBD.
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  Research progress on PD-1 regulating Treg in immune-related pathological processes or diseases

  LUO Zhenjie, GAO Ling, LI Chunfang, CHEN Xiantong, WANG Song

  Current Immunology. 2025, 45(4): 469-474.

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  PD-1 is a highly notable immune checkpoint molecule that plays an important role in tumor immune evasion. Tregs are a subset of T cells that negatively regulate the immune response, and are involved in the immune regulation of immune-related pathological processes or diseases such as tumor microenvironment, inflammatory microenvironment, autoimmune diseases, sepsis, and graft-versus-host disease (GVHD). Studies have shown that PD-1 is expressed not only on tumor cells but also on Tregs. This review summarizes the changes in PD-1 expression, the proportion of Tregs and the immune regulation of PD-1 on Tregs in immune-related pathological processes or diseases, aiming to provide new ideas for the study of these pathological processes or diseases.
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  Research progress on cytoskeletal regulation of NLRP3 inflammasome activation

  QIAN Zhizhi, WANG Man

  Current Immunology. 2025, 45(4): 475-479.

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  Cytoskeleton, an important intracellular structural system, not only maintains the morphology and stability of cells, but also participates in a variety of biological processes within cells. Reserches have found that dynamic changes in the cytoske-leton can influence the assembly and activation process of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammatosome. Specific cytoskeletal components regulate the conformation and localization of NLRP3 inflammatosome by direct interaction, thereby controls the assembly and activity of inflammatosome. In addition, cytoskeletal regulatory factors are able to influence the level of activation of NLRP3 inflammatosome, suggesting the regulatory role of cytoskeleton on NLRP3 inflammatosome. This review summarizes the role of the cytoskeleton in inflammasome regulation, with a particular focus on the NLRP3 inflammasome. 
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  Factors affecting the migration ability of NK cells and their applications

  LUO Mengzhen, YANG Lili, ZHU Mengyuan, MA Jiahui, LI Lin, LIAO Liwei

  Current Immunology. 2025, 45(4): 480-486.

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  NK cells have different immunological characteristics from T cells, as they are not restricted by MHC, nor require antigen presentation before killing activity, which play an important role in tumor immunotherapy. However, during the treatment of solid tumors, the efficacy of NK cells is limited by insufficient infiltration towards tumor tissues. This review summarizes multiple molecules regulating the mobility and migration of NK cells, how the interaction between NK cells and other cells affects NK cell mobility and migration, and the latest strategies for enhancing the infiltrating ability of NK cells, in order to provide theoretical basis and research ideas for improving the cytotherapy effectiveness of NK cell and its derivatives.
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  Research progress on the targeted regulation of macrophage polarization and its correlation with cardiovascular diseases

  BA Anshuai, WANG Yu

  Current Immunology. 2025, 45(4): 487-492.

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  As a key regulator of immune responses, macrophages can be polarized into types M1 and M2 and affect the onset, progression, and treatment of cardiovascular diseases. M1 macrophages, characterized by their pro-inflammatory properties, can exacerbate inflammatory responses and thereby accelerate the development of cardiovascular diseases. In contrast, M2 macrophages, with their anti-inflammatory characteristics, contribute to the recovery from cardiovascular diseases. This review summarizes the correlation between M1/M2 macrophage subtypes and cardiovascular diseases including atherosclerosis (AS), essential hypertension (EH), and myocardial infarction (MI), as well as potential regulatory targets during the M1/M2 polarization process. This review provides a theoretical foundation and new research perspectives for further study and treatment of cardiovascular diseases.