30 November 2025, Volume 45 Issue 6

    

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  Effects of CXCL13-glycosaminoglycan interactions in disease progression and B cell function in mouse EAE mode

  LUO Lingjie, YANG Yuting, WANG Weifang, LIU Zichang, DONG Xiao, WU Yanwei, CHEN Liang

  Current Immunology. 2025, 45(6): 633-644.

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  In order to explore the mechanism of interaction between C-X-C motif chemokine ligand 13 (CXCL13) and glycosaminoglycan in autoimmune diseases, C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptides to establish the experimental autoimmune encephalomyelitis (EAE) model. On the 3rd day post-immunization, the modeled mice were randomly divided into 3 groups: the control group, the group treated with mutant mouse CXCL13 protein which lacked the glycosaminoglycan binding capacity (the mutant group), and the group treated with mouse CXCL13 protein (the wild type group). Corresponding protein intervention was performed respectively. Disease scoring was continued. Flow cytometry was used to detect mouse spleen B cells and plasma cell subsets on day 7 and day 14 post-immunization, and the expressions of IgG and IgM in plasma and CXCL13 in spinal cord and plasma were measured by ELISA. Tissue section and transcriptome sequencing of splenic cells were analyzed. The results showed that the wild type group had delayed onset and significantly lower disease scores than the control group (P=0.031 3), while those of the mutant group was between the control group and the wild type group. On the 7th day after immunization, compared to the control group, both the mutant group (P=0.017 2) and the wild type group (P=0.000 2) showed an increased proportion of germinal center B cells and decreased proportion of plasmablasts (P=0.022 3 in the mutant group, P=0.000 1 in the wild type group); On the 14th  day after immunization, compared to the control group, both the mutant group (P=0.000 5) and the wild type group (P=0.003 1) showed an increased proportion of germinal center B cells, while the proportions of plasmablasts (P=0.005 8 in the mutant group, P=0.027 9 in the wild type group) and plasma cells decreased (P=0.002 1 in the mutant group, P=0.034 5 in the wild type group). On day 14 post-immunization, the plasma subsets basically maintained the same trend as day 7 post-immunization, but the germinal center B subsets composition changed dynamically. The plasma IgM level of the wild type group decreased significantly in the early stage of the immune response (P=0.004 6). However, on day 14 post-immunization, compared to that of the control group, the plasma IgG levels in the mutant group (P=0.006 1) and the wild type group (P=0.001 8) increased significantly. The plasma IgM levels in the mutant group (P=0.012 3) and the wild type group (P=0.009 1) also increased significantly. The plasma IgG affinity detection showed that the affinity between IgG and MOG peptides in the control group was higher than that in the other two groups (P=0.038 0). The myelin staining analysis of the spinal cord lumbar enlargement plane sections showed that the demyelination degree was consistent with the trend of disease scores. The transcriptome sequencing data of splenic cells also showed that over time, the differentially expressed genes in the mutant group were more enriched in the humoral immune pathway. This study suggests that the CXCL13-glycosaminoglycan interaction is involved in the antibody production process and mediates the immune response.
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  The m6A-reading protein YTHDC2 regulates FBLN1 to promote macrophage M1 polarization

  LIU Tingting, YU Yulu, MA Dan, LIU Lili, ZHONG Qiong, ZHAO Guojun

  Current Immunology. 2025, 45(6): 645-655.

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  To study the molecular mechanism by which the N6-methyladenosine (m6A)-reading protein YTHDC2 regulates macrophage M1 polarization, the expression level of YTHDC2 protein was detected in a macrophage polarization model. Next, the expressions of polarization markers was detected in YTHDC2 knockdown M1 macrophages. YTHDC2 knockdown M1 macrophages were constructed, and YTHDC2 knockdown and wild type M1 macrophages were sequenced using Illumina Novaseq JP26000/MGISEQ-T7 sequencing platform to identify the differentially expressed genes of the 2 cell groups. The differentially expressed genes were analyzed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment methods to explore the YTHDC2 regulatory pathway and screen for YTHDC2 downstream target genes. Cellular experiments were used to reveal the role of YTHDC2 downstream target gene fibulin 1 (FBLN1) in M1 macrophages. The results showed that YTHDC2 expression was elevated in M1 macrophages. Expression levels of polarization markers were decreased in YTHDC2 knockdown M1 macrophages. 147 differentially expressed genes were identified between YTHDC2 knockdown and wild type M1 macrophages. FBLN1 expression is up-regulated in YTHDC2 knockdown M1 macrophages. Potential m6A methylation might occur at multiple sites in FBLN1. Expression levels of polarization markers were increased in M1 macrophages with the knockdown of YTHDC2 and FBLN1. In conclusion, YTHDC2 may promote macrophage M1 polarization by regulating the m6A modification of FBLN1.
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  CD83⁺B cells are enriched in atherosclerotic plaques and exhibit a senescent phenotype

  LIU Kai, PAN Zihe, ZHAO Pengyuan, XUE Ruilu, WANG Zhiqiang, LIU Ronghua

  Current Immunology. 2025, 45(6): 656-663.

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  This study aimed to identify the B cell phenotypic characteristics in atherosclerotic plaques and explore the potential relationship between B cells and plaque inflammation progression. By comparing the immune cell profiles from single-cell sequenicing data of plaques and peripheral blood in atherosclerotic patients, 2 CD83⁺B cell clusters enriched in human atherosclerotic plaques were identified, with increased percentages of 46.74% and 19.18%, respectively. Compared to other B cell subpopulations, CD83⁺B cells expressed higher levels of aging-related genes including CDKN1A, IL-6, TNF-α, MALAT1, and GADD45B, suggesting that the increased CD83⁺B cells in plaques exhibited a senescent phenotype. To validate these findings, ApoE gene knockout (ApoE^-/-) mice were fed with Western diet (WD) to induce atherosclerosis. The proportion of CD83⁺ B cells in total B cells was significantly higher in the arterial tissues of WD mice (fold change=5.36，P=0.010 8). Consistently, in WD mice, the average fluorescence intensities of senescence-associated inflammatory cytokines including IL-6, TNF-α, and IFN-γ in CD83⁺B cells were significantly higher than those of the CD83^-B cells, with significant fold changes of 1.95 (P=0.020 2), 4.25 (P=0.003 0), and 4.20 (P=0.016 9), respectively. This study reveals that CD83⁺B cells are enriched in atherosclerotic plaques and exhibit a senescence-like phenotype, producing higher levels of senescence-associated inflammatory factors that may contribute to arterial inflammation.
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  Molecular mechanism of CCL3-mediated ferroptosis in alveolar epithelial cells via the NF-κB signaling pathways in regulating sepsis-induced acute lung injury

  LUO Hui, LI Xiaofei

  Current Immunology. 2025, 45(6): 664-671.

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  To investigate the effect of targeted knockdown of C-C motif chemokine ligand 3 (CCL3) expression in alleviating sepsis-induced acute lung injury (ALI) and the underlying mechanism, an induced mouse sepsis model was established by cecal ligation and puncture (CLP). Lung tissue samples were collected, and differentially expressed genes and enriched pathways were identified by RNA sequencing (RNA-seq） analysis. Small interfering RNA (siRNA) technology was used to specifically knockdown the expression of the key gene CCL3, and si-CCL3 plasmids were injected via the tail vein for in vivo intervention. Mice were randomly divided into 3 groups according to the experimental design: the sham operation control group, the sepsis model group, and the si-CCL3 silencing group. H-E staining was used to evaluate the degree of lung tissue pathological damage, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was used to detect the level of cell apoptosis. The results showed that the sepsis mouse model was successfully established by CLP. RNA-seq results indicated that compared with the control group, there were 475 up-regulated genes and 467 down-regulated genes in the lung tissue of sepsis mice, among which the up-regulation of CCL3 was the most significant. The relative expression of CCL3 mRNA in mouse lung tissue was detected by qRT-PCR, and the results were consistent with those of the RNA-seq, showing that CCL3 was significantly up-regulated in the lung tissue of mice with sepsis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment pathway analysis results showed that the NF-κB signaling pathway and ferroptosis marker proteins glutathione peroxidase 4 (GPX4) and prostaglandin-endoperoxide synthase 2 (PTGS2) were all involved in the process of sepsis-induced ALI. The results of qRT-PCR and Western blotting were consistent with RNA-seq results. After treatment with si-CCL3 plasmids, the pathological changes in the lung tissue were significantly improved, the structure of bronchi and alveoli was significantly restored, the thickness of alveolar septum was reduced, and interstitial exudation was decreased. TUNEL staining results showed that the number of apoptotic cells in the si-CCL3 silencing group was significantly lower than that of the sepsis model group (P<0.05). In conclusion, targeted knockdown of the chemokine CCL3 expression can alleviate the process of sepsis-associated acute lung injury by inhibiting the ferroptosis phenotype in lung tissue.
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  Construction of conditional macrophage Gpr84 knockout mice and the functional study in acute lung injury

  SHEN Kairui, HOU Ruitao, LIU Jiannan, XUE Mengfei, REN Hua, QIN Juliang, DU Bing, SUN Zhengliang

  Current Immunology. 2025, 45(6): 672-678.

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  To investigate the regulation of the G protein-coupled receptor 84 (GPR84) of macrophages and its role in acute lung injury, CRISPR/Cas9 gene editing technology was used to construct Gpr84 conditional knockout mice (Gpr84^loxp/loxp), which were subsequently hybridized with macrophage-specific Lyz2-Cre mice to generate the macrophage Gpr84 conditional knockout (cKO) mice. Next, the acute lung injury model was established by a single intratracheal administration of LPS (5 mg/kg) to the conditional knockout and C57BL/6 wild-type (WT) mice. The mice were divided into 4 groups: the WT-control, the cKO-control, the WT-LPS, and the cKO-LPS groups, with 6 animals in each group. The cKO mice were identified using PCR technology. H-E staining was employed to examine the pathological changes in lung tissue. The ratio of wet weight/dry weight (W/D) was measured in lung tissue, and qRT-PCR was utilized to quantify the expression of inflammatory factors, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase 1 (Hmox1) in lung tissue. ELISA was used to determine the levels of IL-1β, IL-6, and MCP-1 in mouse serum, and immunohistochemistry was performed to detect the protein level of Nrf2 in lung tissue. The results showed that the macrophage Gpr84 knockout mice were successfully constructed, and the function of GPR84 in acute lung injury was studied. Compared to the control group, the LPS group exhibited significant inflammatory cell infiltration and alveolar collapse, increased lung injury scores, elevated lung W/D ratio, and increased expression of inflammatory factors in lung tissue and serum. However, compared to the WT-LPS group, the cKO-LPS group showed reduced pulmonary inflammatory cell infiltration, decreased lung injury scores, and significantly reduced expression of inflammatory factors in lung tissue and serum. In addition, the expressions of Nrf2 and Hmox1, which have antioxidant functions, significantly increased. This study suggests that the specific knockout of the Gpr84 gene in macrophages can significantly alleviate LPS-induced lung inflammation and enhance the resistance to oxidative stress, indicating that GPR84 may serve as a potential target for the treatment of acute lung injury.
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  Efficacy study of human umbilical cord blood mesenchymal stem cells on  immune thrombocytopenia mouse

  YANG Baojuan, YANG Min, WU Xinhua

  Current Immunology. 2025, 45(6): 679-686.

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  The aim of the study was to investigate the effect of human umbilical cord blood mesenchymal stem cell (hUC-MSC) on immune thrombocytopenia (ITP) mouse model and its regulation on the retinoic acid-related orphan receptor γt (ROR-γt)/forkhead winged helix transcription factor 3 (Foxp3) signaling pathway. Healthy hUC-MSCs were isolated and cultured, the growth patterns were observed and identified, and the stably-proliferating primary cells were selected for passaging. Thirty male BALB/c mice were randomly divided into the normal control group (Con group), the ITP model group and the hUC-MSC group, with 10 mice in each group. After corresponding treatments, the general condition of the mice was observed. Peripheral platelet count (PLT) was measured, and serum levels of IL-6, IL-17, IL-10, and TGF-β1 were detected using ELISA. Wright-Giemsa staining was used to evaluate the pathological changes in mouse bone marrow and to count the megakaryocytes. Western blotting and RT-qPCR were used to detect protein and mRNA levels of ROR-γt and Foxp3 in mice spleen and peripheral blood, respectively. The results showed that compared to those of the Con group, the serum IL-6 and IL-17 levels, ROR-γt mRNA and protein expression in spleen and the ROR-γt mRNA and protein expression in peripheral blood were all significantly higher in the ITP model group (all with P＜0.05), while the PLT, serum IL-10 and TGF-β1 levels, Foxp3 mRNA and protein expression in spleen and Foxp3 mRNA and protein expression in peripheral blood were significantly decreased (all with P＜0.05), along with significantly reduced number of platelet-producing megakaryocytes (P＜0.05). Compared to the ITP model group, the hUC-MSC group showed significantly lower serum IL-6 and IL-17 levels, splenic ROR-γt mRNA and protein expression and peripheral blood ROR-γt mRNA and protein levels (all with P＜0.05), but significantly higher PLT, serum IL-10 and TGF-β1 levels, splenic Foxp3 mRNA and protein expression, peripheral blood Foxp3 mRNA and protein expression (all with P＜0.05), and the elevated number of platelet-producing megakaryocytes (P＜0.05). As a result, hUC-MSC can promote platelet formation and increase the number of platelet-producing megakaryocyte, which may relief the symptoms of ITP mice by regulating the expressions of cytokines and the ROR-γt/Foxp3 axis.
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  Research on the regulation of JAK2/STAT3 signaling by m6A-modified SOCS2 in the intervention of colorectal cancer progression

  LIU Pan, CHEN Yali, XU Weiwei

  Current Immunology. 2025, 45(6): 687-694.

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  The study aimed to explore the regulation of N6-methyladenosine (m6A) modification of SOCS2 on the progression of colorectal cancer via the JAK2/STAT3 signaling pathway and the possible underlying mechanism. Human normal colon epithelial cell NCM460 and human colon cancer cells SW480, LOVO, HCT-15, HT-29, and SW1116 were cultured, and the overall level of m6A RNA was detected. Western blotting and RT-qPCR were used to detect METTL3 protein and mRNA levels, respectively, and SELECT-qPCR modified quantitative technique was used to detect the m6A level at SOCS2 site. LOVO and HT-29 cells were divided into the control group (WT cells) and the METTL3 low expression group (transfection with low-expression METTL3 plasmid). SOCS2 levels in LOVO and HT-29 cells were detected by immunofluorescence staining. Western blotting was used to detect the expression levels of JAK2, STAT3, p-JAK2 and p-STAT3 in LOVO and HT-29 cells. Plate clone formation assay was used to detect the clone-forming ability of LOVO and HT-29 cells, and scratch assay was used to detect the migration of LOVO and HT-29 cells. The invasive ability of LOVO and HT-29 cells was detected by the Transwell assay. The results showed that, compared to those of NCM460, the overall levels of m6A RNA in all the cancer cell lines were increased (P<0.05, P<0.01), and the protein and mRNA levels of METTL3 in LOVO and HT-29 cells were also increased (P<0.01). The m6A level of SOCS2 was increased (P<0.05). Compared to that of the control group, the expression of SOCS2 in LOVO and HT-29 cells in the METTL3 low expression groups were increased (P<0.01), while the expression of METTL3 protein and mRNA were decreased (P<0.01), and no significant changes in JAK2 and STAT3 (P>0.05) were observed. The expressions of p-JAK2 and p-STAT3 were decreased (P<0.01), and the proliferation, migration, and invasion abilities of LOVO and HT-29 cells were also decreased (P<0.01). This study indicates that low expression of METTL3 can downregulate JAK2/STAT3 signaling pathway and inhibit the proliferation, migration, and invasion of colon cancer cells, which may be related to the regulation of JAK2/STAT3 signaling pathway by m6A modification of SOCS2.
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  Expressions of NCAPD2 and ADAM17 in colon cancer tissues correlate with patient prognosis

  HAN Yuefeng, JIANG Xuefeng, WANG Yunchun, YUAN Mingtuan, YANG Qian

  Current Immunology. 2025, 45(6): 695-701.

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  The study aims to analyze the expressions of non-structural maintenance of chromosome condensin Ⅰ complex subunit D2 (NCAPD2) and a disintegrin and metalloprotease 17 (ADAM17) in colon cancer tissues and the correlation with patient prognosis. One hundred colon cancer patients subjected to radical resection surgery were selected. During the surgery, colon cancer tissue specimens and normal tumor-adjacent tissue specimens with a distance of more than 5 cm from the colon cancer tissue were collected from the patients. The expression levels of NCAPD2 and ADAM17 in the two types of specimens were detected by Western blotting, and the expressions of NCAPD2 and ADAM17 in patients with different clinical and pathological characteristics were analyzed. The patients were followed up for 3 years and their survival data were recorded. The pateints were divided into the survival group (67 cases) and the death group (33 cases). The expression levels of NCAPD2 and ADAM17 were compared between the two groups. ROC curve was used to evaluate the predictive value of NCAPD2 and ADAM17 for the prognosis of colon cancer patients. The cut-off value in the curve was used as the threshhold for NCAPD2 and ADAM17 expressions, which was used to divide patients into high expression and low expression groups. Meanwhile, Kaplan-Meier survival curve was used to compare the survival of the two groups. The results showed that the expression levels of NCAPD2 and ADAM17 in colon cancer tissues were higher than those in normal tissues (P<0.001). The expression levels of NCAPD2 and ADAM17 in patients with infiltration degree T3-T4, low differentiation, distal metastasis, and lymph node metastasis were higher than those in the corresponding control group (P<0.05). The expression levels of NCAPD2 and ADAM17 in the death group were higher than those in the survival group (P<0.05). The ROC curve showed that the AUC of NCAPD2 and ADAM17 for predicting death were 0.780 and 0.721, respectively. The Kaplan-Meier survival curve showed that the survival time of patients with high expressions of NCAPD2 and ADAM17 was significantly shorter than that of patients with low NCAPD2 and ADAM17 expressions (P<0.001). The study suggests that NCAPD2 and ADAM17 are highly expressed in colon cancer tissues, and are highly correlated to the invasion, metastasis and prognosis of colon cancer, underscoring their significance in the prognosis assessment of colon cancer patients.
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  Dihydroartemisinin alleviates depressive-like behavior in mice by inhibiting inflammatory response in the hippocampus via the complement C3/C3aR signaling pathway

  LIU Yutong, XU Jiaqi, JIN Peiang, XIAO Bin

  Current Immunology. 2025, 45(6): 702-709.

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  This study explores the potential mechanism by which dihydroartemisinin (DHA) modulates the complement C3/C3a receptor (C3aR) signaling pathway to improve neuroinflammation in the hippocampus in a mouse depression model. Forty male C57BL/6J mice aged 8 weeks were randomly divided into 4 groups: the control group, the model group, the low-dose DHA (DHA-L) group, and the high-dose DHA (DHA-H) group, with 10 mice in each group. Except for the control group, the remaining groups were subjected to chronic unpredictable mild stress (CUMS) to establish the depression model. Behavioral assays were performed to evaluate the success or failure of the model and changes in depressive behaviors in the mice. H-E staining and Nissl staining were used to assess neuronal pathological damage in the hippocampus. ELISA was employed to detect inflammatory cytokine levels, while immunohistochemistry was used to observe microglial activation. Western blotting was performed to detect the expression levels of C3 and C3aR proteins. The results showed that the depression model in mice was successfully established. Mice in the model group showed a significant decrease in sucrose preference, time spent in the center of the open field, and total distance traveled in the open field compared to the control group (P<0.01). In the tail suspension and forced swimming tests, the immobility time of modeled mice was significantly prolonged (P<0.001). Mice in the DHA-L group and the DHA-H group showed a significant increase in sucrose preference, time spent in the center of the open field, and total distance traveled compared to the model group (P<0.05). Furthermore, their immobility time in the tail suspension and forced swimming tests was significantly reduced (P<0.05). The inflammatory cytokine levels in the hippocampus of the model mice were significantly higher than those in the control group (P<0.01), and DHA treatment significantly reversed this effect (P<0.05). DHA treatment also alleviated the pathological damage to hippocampal neurons in the model mice. The number of activated microglia in the hippocampus of the model group was significantly increased compared to that of the control group (P<0.001), whereas DHA treatment significantly reduced microglial activation compared to the model group (P<0.05). The expression levels of C3 and C3aR in the hippocampus of model mice were significantly higher than those in the control group (P<0.01), and DHA treatment significantly downregulated the expression of these proteins (P<0.05). In conclusion, the antidepressant effect of DHA may be mediated by reducing neuroinflammation in the hippocampus, and the mechanism is likely associated with the C3/C3aR signaling pathway.
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  Inhibition of icariin on apoptosis of retinal cells in rats with diabetic retinopathy via the SIRT1/FOXO3a/NF-κB signaling pathway

  HAN You, WANG Min, ZHAO Junbo, LI Jiajia, CUI Cui

  Current Immunology. 2025, 45(6): 710-716.

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  The aim of the study is to investigate the effects of icariin on apoptosis of retinal cells in diabetic retinopathy (DR) rats through the silent mating-type information regulation 2 homolog 1 (SIRT1)/forkhead-box transcription factor O3a (FOXO3a)/NF-κB signaling pathway. The SD rats were randomly divided into the control (Ctrl), the DR, the low-dose icariin (L-icariin), the high-dose icariin (H-icariin), and the SIRT1 inhibitor + H-icariin groups. The DR rat model was established by intraperitoneal injection of streptozotocin (STZ) combined with high-sugar+high-fat diet. Serum levels of oxidative stress markers (superoxide dismutase ［SOD］ and malondialdehyde ［MDA］), and inflammatory factors (TNF-α and IL-6) were measured. Retinal histopathological changes were observed by H-E staining. Retinal cell apoptosis was assessed by TUNEL assay. B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) expressions were detected by immunohistochemistry. Western blotting was used to analyze the protein expressions of SIRT1 and acetylated NF-κB (ac-NF-κB). Immunoprecipitation (IP) was used to detect ac-FOXO3a protein expression in retinal tissue. The results showed that compared with the Ctrl group, the DR group exhibited reduced serum SOD level and increased expressions of MDA, TNF-α, and IL-6 (all with P＜0.05). Retinal cells displayed disordered arrangement and were significantly decreased in number, accompanied by cellular edema and nuclear shrinkage. The apoptosis rate of retinal cells was increased (P＜0.05), along with decreased Bcl-2 and increased Bax protein expressions in retinal tissue (all with P＜0.05). After intervention with L-icariin or H-icariin, these abnormalities were mitigated, with the H-icariin group showing better efficacy. Compared with the Ctrl group, the DR group demonstrated reduced SIRT1 protein expression and increased ac-FOXO3a and ac-NF-κB protein expressions (all with P＜0.05) in retinal tissue. Both H-icariin intervention and concurrent SIRT1 inhibitor treatment diminished or reversed these protein expression profiles. Notably, SIRT1 inhibitor reduced the effect of icariin on retinal cell apoptosis. These findings suggest that icariin may alleviate retinal lesions and inhibit retinal cell apoptosis in DR rats through regulating the SIRT1/FOXO3a/NF-κB signaling pathway.
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  The regulation of cryptotanshinone on neuroinflammation in schizophrenia rats via the NLRP3/Caspase-1 signaling pathway

  WANG Guangkuo, PAN Yuhong, LIU Jia

  Current Immunology. 2025, 45(6): 717-722.

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  The study aims to investigate the effects of cryptotanshinone (CTS) on neuroinflammation in schizophrenia (SP) rats. SD rats were randomly divided into the control group, the model group, the low-dose CTS group (15 mg/kg), the medium-dose CTS group (30 mg/kg), the high-dose CTS group (60 mg/kg), and the activator group (60 mg/kg CTS+10 mg/kg NOD-like receptor family pyrin domain-containing protein 3 ［NLRP3］/Caspase-1 signaling pathway activator BMS-986299), with 12 animals per group. The SP rat model was constructed by intraperitoneal injection of dizocilpine in all groups except the control group. H-E staining was used to observe the pathological damage of hippocampal tissue. ELISA was used to detect the expression levels of serum IL-6 and TNF-α. The activities of hippocampal tissue acetyl choline (dihydrokaempferol, Ach) and acetyl cholinesterase (AchE) were measured using commercial kits. qRT-PCR was used to detect NLRP3, Caspase-1 mRNA expression; Western blotting was used to detect NLRP3/Caspase-1 signal pathway related protein expressions. The results showed that, compared to the control group, the model group had less obvious structural hierarchy, sparser cell arrangement, wrinkled cytosol morphology, increased expressions of IL-6, TNF-α, AchE, increased mRNA and protein levels of NLRP3 and Caspase-1, and decreased Ach level (P<0.05). Compared to those of the model group, the cellular structural hierarchy and morphology in the low-dose CTS group, the medium-dose CTS group, and the high-dose CTS group all showed  dose-dependent improvement, as well as decreased expressions of IL-6, TNF-α, AchE, mRNA and protein levels of NLRP3 and Caspase-1 and increased Ach (P<0.05). Compared to the high-dose CTS group, the activator group showed aggravated cellular structural hierarchy and morphological changes, increased expression levels of IL-6, TNF-α, AchE, mRNA and protein levels of NLRP3 and Caspase-1, and decreased Ach (P<0.05). This study suggests that CTS may ameliorate neuroinflammation in SP rats by inhibiting the NLRP3/Caspase-1 signaling pathway.
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  A method for rapid intraoperative determination of lymph node metastasis characteristics in thyroid papillary carcinoma surgery

  SHI Longshun, MA Qi, YANG Runlin, FENG Feiyu, GUO Mingming, FAN Jun, LYU Zhongwei, ZHOU Bin

  Current Immunology. 2025, 45(6): 723-727.

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  To facilitate the prompt identification of thyroid cancer lymph node metastasis during surgery, this study developed a method for the quick and accurate determination of thyroid globulin (Tg) content in intraoperative cervical lymph node puncture fluid using fine-needle aspiration (FNA) combined with lateral flow time-resolved immunofluorescence assay. A time-resolved fluorescence immunochromatographic assay for Tg in tissue fluid was established, and the performance was validated. The optimal intraoperative sampling method for cervical lymph node tissue fluid was established, and reference values were determined based on pathological results to verify clinical feasibility. The developed rapid Tg detection method demonstrated excellent stability and precision within a 15-minute detection window, with intra-assay and inter-assay coefficients of variation at 8.38% and 11.24%, respectively. It exhibited high sensitivity, detecting concentrations as low as 0.02 ng/mL, and high specificity without cross-reactivity with TPO. The sampling protocol involved 6 punctures in all directions of the lymph node using a 26-gauge needle, with repeated aspiration and injection 3 times into the sample preservation solution. Using 7.36 ng/mL as the reference value and comparing it with pathological results, the clinical positive coincidence rate was 95.16%, and the negative coincidence rate was 96.47%. The above results indicate that the rapid Tg detection method via FNA of lymph node tissue fluid is clinically feasible and effective for identifying the nature of thyroid cancer lymph node metastasis during surgery.
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  Exploration of the mechanism and potential therapeutic prospects of exosomal microRNA in rheumatoid arthritis

  ZHANG Ying, YI Guoxiang, WANG Jing, WANG Miao

  Current Immunology. 2025, 45(6): 728-735.

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  Rheumatoid arthritis (RA) is a chronic autoimmune disease that can lead to joint deformity and loss of function. Due to the complexity of pathological mechanism and diversity of inflammatory cytokines, current treatments still lacks clinical efficacy and new treatment strategies have been continuously explored internationally. There is evidence suggesting that exosome and the miRNA encapsulated in them are involved in the pathogenesis of RA. Exosomal miRNA show great potential as biomarkers for the diagnosis of RA and as diagnostic tools for accurate identification and target therapy. As the most promising drug delivery vector, exosomes are expected to become one of the new treatment methods for RA. In recent years, researchers have conducted in-depth studies on the role of exosomal miRNA in the pathogenesis and progression of RA. This review summarizes the research progress on the mechanism of exosomal miRNA involved in RA pathogenesis and explores their potential clinical application prospect.
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  Research progress on metabolic regulation of macrophage phenotype

  JIANG Zhiyue, HE Jiali, CUI Shuna

  Current Immunology. 2025, 45(6): 736-741.

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  Macrophages are innate immune cells that mainly play roles in antigen presentation and phagocytosis. Macrophages are categorized to M1 and M2 types. M2 macrophages in different microenvironments can be further divided into 4 subtypes: M2a, M2b, M2c, and M2d. M1 macrophages are induced by IFN-γ and LPS, which promote inflammation, inhibit microbial and tumor growth while M2 macrophages are activated by IL-4 or IL-13, and have anti-inflammatory activity, and their functions include tissue homeostasis maintanence, immune regulation, phagocytosis, promoting angiogenesis, and influencing tumor formation and progression. The special functions of various phenotypes of macrophages are mainly controlled by polarization signals, which can activate macrophages by upregulating different transcription programs. This review focuses on the relationships between the three metabolic pathways (sugar metabolism, lipid metabolism and amino acid metabolism) and the polarization of different macrophages which provides new solutions for diseases related to macrophage polarization.
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  Research progress on interleukin 17D

  ZHAO Junli, GU Xiaodong, WENG Ruiqiang, LI Xia, LIU Sudong

  Current Immunology. 2025, 45(6): 742-746.

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  IL-17D is a member of the IL-17 cytokine family which consists of 6 members, including IL-17A to IL-17F. The IL-17 receptor （IL-17R） family consists of 5 members: IL-17RA to IL17RE. IL-17A, as the typical representative of the IL-17 family and a hallmark cytokine produced by Th17 cells, plays a significant role in autoimmune diseases, tumorogenesis and inflammatory response. Although IL-17D is similar to IL-17A in the potential to elicit inflammatory cytokine production, studies on IL-17D are relatively fewer compared to those of IL-17A, and its function and mechanism of action remain elusive. In recent years, it has been found that IL-17D plays an important role in various diseases such as inflammatory response, viral infection, tumor and cardiovascular diseases, etc. By interacting with receptors on the surface of target cells, IL-17D activates downstream signaling pathways, regulates the expression of inflammatory factors, chemokines, etc., and participates in the recruitment and activation of immune cells. In addition, IL-17D has potential therapeutic value in antiviral immunity and tumor immunosurveillance. The review summarizes the structural features, biological activity and expression of IL-17D and its correlation with diseases.
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  Review on the pathogenesis of GD-IgA1 in pediatric IgA vasculitis

  LEI Hong, SONG Lei, YUAN Yinglun, HU Tianle, WEI Xia, XU Yan, GUO Linmei, DAI Yongli

  Current Immunology. 2025, 45(6): 747-753.

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  IgA vasculitis (IgAV) is a common vasculitis syndrome during childhood and is considered a self-limiting disease. While its pathogenesis remains largely elusive. The short-term symptoms primarily involve skin, gastrointestinal tract and joint burden, with a generally favorable prognosis. However, in the long course, severe renal damage can progress to renal failure. Therefore, investigating the pathogenesis of IgAV is crucial for preventing the disease and managing related organ damage. Accumulating evidences indicate a strong correlation between galactose-deficient IgA1 (GD-IgA1) and the occurrence of IgAV. This review comprehensively discusses the relationship between GD-IgA1 and pediatric IgAV and  firstly  elucidates the central role of GD-IgA1 in IgAV pathogenesis from multiple dimensions, including genetics, immune cells, infection, and the gut microbiota. This review also elaborates the mechanisms underlying the formation and deposition of immune antibody complexes and their sequential damage to kidney and gastrointestinal tract which provide a theoretical foundation for deeper understanding of the disease pathogenesis and the development of glycosylation targeted and microbiome-based interventions.
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  Advances in the immunoregulatory effects of β-glucan

  WENG Nan, WU Jing, TAO Yue

  Current Immunology. 2025, 45(6): 754-758.

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  β-glucan is a natural polysaccharide widely existed in cereals, bacteria, and fungi. In recent years, β-glucan has attracted much attention due to its broad immunomodulatory effects. It can directly modulate neutrophils, monocytes, and macrophages, leading to their metabolic and epigenetic reprogramming and exerting a direct modulatory effect on intrinsic immunity. Besides, it can also impact the differentiation of T and B cells and the release of inflammatory factors to regulate adaptive immunity. In addition, β-glucan has been reported to influence the body's immune response by regulating gut flora. This review summarizes the immunomodulatory effects and mechanisms of β-glucan, as well as the clinical applications of β-glucan in tumors, allergic diseases, infectious diseases, and other types of diseases. This review will provide a theoretical reference and scientific basis for the further development and utilization of β-glucan.