30 May 2025, Volume 45 Issue 3

  

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  The regulation of apolipoprotein A IV on renal macrophages in obese mice

  ZHANG Ting, WANG Yiying, WEI Yang

  2025, 45(3): 249-258.

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  Obesity-induced metabolic disorders, immune dysregulation, and metainflammation promote the pathogenesis and progression of chronic kidney disease (CKD). Apolipoprotein A IV (ApoA-IV) is a lipid-binding protein that regulates gluco-lipid metabolism and exhibits anti-inflammatory activity. However, the impact of ApoA-IV on the immune microenvironment of obesity-related chronic kidney inflammation remains insufficiently explored. This study employed the high-fat diet (HFD) to establish the HFD-induced obesity (DIO) model in both ApoA-IV knockout (ApoA-IV-/-/ApoA-IV KO) and wild type (WT) mice.The results showed that ApoA-IV KO exacerbated insulin resistance and renal lipid accumulation in DIO mice. Further analysis of the single-cell RNA sequencing (scRNA-seq) of kidney tissue and of immune cells revealed that ApoA-IV KO increased oxidative stress in macrophages, aggravated inflammations, impaired macrophage differentiation and polarization of M1- and M2-type phenotypes, reduced antigen processing，presentation and phagosome biological proceedings. Furthermore, ApoA-IV KO weakened the intercellular immune communication. It particularly downregulated the input signaling to macrophages, including pro-inflammatory IFN-II and TNF signaling, and the pro-proliferation and differentiation signaling including CSF and FLT3. Output signaling from macrophages were meanwhile downregulated, including immune-suppressive GALECTIN signaling, pro-resolving ANNEXIN signaling and immune-activating SPP1 signaling. Flow cytometry and bulk RNA sequencing of kidney tissue partially validated the scRNA-seq findings. This study highlights the critical role of ApoA-IV in regulating macrophage differentiation, functioning, oxidative stress, and inflammatory responses in the obese kidney, providing new insights for further exploration of the immune mechanisms underlying chronic kidney inflammation.
  
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  Expression of lncRNA FGD5-AS1 in hepatocellular carcinoma and its effects on proliferation, migration, and invasion of Huh-7 cells

  DAI Zhiqiang, TANG Fuxing, YANG Jing

  2025, 45(3): 259-270.

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  In order to investigate the expression of long non-coding RNA (lncRNA) containing antisense RNA1 for 5 PH domains (FGD5-AS1) in hepatocellular carcinoma (HCC) tissues, its effects and mechanism on proliferation, migration, and invasion of HCC cells, HCC tissues and corresponding adjacent tissues of 53 HCC patients were collected.Human HCC cell lines (Hep3B, SK-HEP-1, MHCC97L, MHCC97-H, and Huh-7) and normal human hepatocytes (LO2) were cultured in vitro. RT-qPCR was used to detect the expression levels of lncRNA FGD5-AS1 and miR-512-3p in tissues and cell lines and the correlation between the expression levels of FGD5-AS1 and miR-512-3p in HCC patients' cancer tissues were analyzed by Pearson correlation test.Western blotting was used to detect the expression of Cyclin D1 protein. HCC cell line Huh-7 was cultured in vitro, and was transfected with FGD5-AS1 small-interfering RNA (siRNA) or miR-512-3p mimic, respectively, or co-transfected with FGD5-AS1 siRNA and miR-512-3p inhibitor. The proliferation, migration, and invasion of cells in each group were detected by CCK8 assay, cell cloning experiment and Transwell assay, respectively. The dual-luciferase reporter gene experiment was used to verify the binding between FGD5-AS1 and miR-512-3p or miR-512-3p and Cyclin D1. FGD5-AS1 knockdown (KD) Huh-7 cells were subcutaneously inoculated into nude mice to observe tumor growth. The results showed that compared to those of the adjacent tissues, the protein expressions of FGD5-AS1 and Cyclin D1 were increased in HCC tissues (both P＜0.05), while the expression of miR-512-3p was decreased (P＜0.05). There was a significant negative correlation between FGD5-AS1 and miR-512-3p levels in HCC tissues (r=-0.856, P＜0.01). Compared to those of the LO2 cells, the protein expressions of FGD5-AS1 and Cyclin D1 in human HCC cell lines (Hep3B, SK-HEP-1, MHCC97L, MHCC97-H, and Huh-7) were all increased, while the expression level of miR-512-3p was decreased (all with P＜0.05). FGD5-AS1 KD or over-expression of miR-512-3p reduced the proliferative activity, number of colony formation, migration, and invasion of Huh-7 cells (all with P＜0.05). FGD5-AS1 targeted miR-512-3p, and the expression of miR-512-3p was increased in Huh-7 cells upon FGD5-AS1 KD (P＜0.05). Cyclin D1 was the target gene of miR-512-3p, and the expression of Cyclin D1 protein was decreased in Huh-7 cells overexpressing miR-512-3p (P＜0.05). Down-regulation of miR-512-3p reversed the inhibition of FGD5-AS1 KD on Huh-7 cells proliferation, migration, invasion, and Cyclin D1 expression. Xenografted nude mice result demonstrated that FGD5-AS1 KD inhibited the growth of Huh-7 cells in vivo. In conclusion, lncRNA FGD5-AS1 is highly expressed in HCC tissues and FGD5-AS1 KD inhibits the proliferation, migration, and invasion of Huh-7 cells by targeting the miR-512-3p/Cyclin D1 axis. 
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  Preparation and identification of monoclonal antibody specific to the P2 substructural domain of GⅡ.17 type norovirus

  DENG Shiyuan, TANG Qiuyang, WANG Bin, DENG Jianping, MING Xuewei, DU Yunxiao, XIE Yongmei, LI Zaixin, ZHANG Zhi

  2025, 45(3): 271-277.

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  The aim of this study was to prepare a monoclonal antibody targeting the P2 substructural domain of the GⅡ.17 type norovirus (NV) using recombinant protein immunization-hybridoma technique, and to characterize its biological properties. The purified recombinant antigen GⅡ.17-P2 was used to immunize BALB/c female mice, followed by cell fusion of SP2/0 and splenocytes from the immunized mice using the hybridoma technique. A specific antibody positive hybridoma cell line was selected for the production and purification of the monoclonal antibody specific to the substructural domain of the P2 region of GⅡ.17 NV. The biological characteristics of the monoclonal antibody were subsequently evaluated by indirect ELISA, Western blotting, and dot-ELISA assays. Additionally, the sequences of the variable regions of the monoclonal antibody were examined by semi-nested PCR. The results showed that a total of 23 positive hybridoma cell lines were acquired, with a positivity rate of 23.96%. A cell line stably secreting the monoclonal antibody specific to GⅡ.17 type NV P2 domain, named G10, was obtained by subcloning and other techniques. G10 monoclonal antibody was prepared from ascites by antibody purification. The G10 monoclonal antibody had a titer of up to 10-5 μg/mL, a sensitivity of 10-5 μg/mL for antigen detection by means of ELISA, and can recognize the wild-type GⅡ.17 NV. The sequence characteristics of the variable regions of the G10 monoclonal antibody were also elucidated. In brief, monoclonal antibody targeting the P2 substructural domain of GⅡ.17 NV has been successfully developed by the recombinant protein immunization-hybridoma technology, laying the foundation for the development of rapid diagnostic reagents against GⅡ.17 type NV.
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  Protective effect and mechanism of ginkgolide B on ulcerative colitis mice model

  LIANG Jianyun, XU Jinsong, JIN Ailian, ZHAO Rui

  2025, 45(3): 278-283.

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  To investigate the protective effect and underlying mechanism of ginkgolide B against trinitrobenzenesulfonic acid（TNBS）-induced ulcerative colitis (UC) in mice, this study used 60 specific pathogen free grade male C57BL/6 mice randomly divided into 6 groups: the control group, the UC model group, the ginkgolide B low-dose group (2.5 mg/kg), the ginkgolide B medium-dose group (5 mg/kg), the ginkgolide B high-dose group (10 mg/kg), and the sulfasalazine group (100 mg/kg). The UC model was established by slowly injecting TNBS solution into the mouse colon through a flexible catheter. The severity of UC was assessed by body weight, colon length, and disease activity index (DAI). Histological changes were observed by H-E staining and the expressions of inflammatory factors were detected by ELISA.The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) were detected by corresponding activity measuring kits. The protein expressions of the TLR4/NF-κB pathway were detected by Western blotting. The results showed that, compared to the model group, mice in both the ginkgolide B medium- and high-dose groups showed less weight loss, longer colon length, lower DAI scores, significantly improved pathological damage of colitis, significantly lower expressions of TNF-α, IL-1β, IL-6, IL-2, and IL-12, significantly higher expression of IL-10, higher levels of SOD and GSH-Px, and lower levels of MDA. In addition, the activation of proteins in the TLR4/NF-κB pathway were inhibited. In summary, ginkgolide B has a significant protective effect on UC, and the mechanism may be related to the inhibition of the activation of TLR4/NF-κB signaling pathway.
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  Effect of human mesenchymal stem cells with high expressions of both IL-18 and IL-12 on the in vitro expansion of peripheral NK cells

  LI Jinglin, XU Xiaomeng, MENG Shiyu, TANG Yijun, WANG Fenhong, WU Hailian, CHEN Xin, JIN Xinyu, XUE Binghua

  2025, 45(3): 284-290.

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  In order to evaluate the effect of human mesenchymal stem cells with high expressions of both IL-18 and IL-12 on the in vitro expansion of NK cells from human peripheral blood, IL-18 and IL-12 high expression mesenchymal stem cells were constructed and used as feeding layers in activated culture flasks. PBMCs of healthy humans were collected and cultured in the activation flasks, and a cytokine induced culture protocol was used as the control. Growth curve of NK cell was statistically analyzed. Flow cytometry was used to analyze the proportion of NK cells and K562 cells were used as target cells to examine the in vitro killing ability of NK cells of the stem cell and the control groups. The results showed that the expansion efficiency of NK cells in the absolute ethanol fixed mesenchymal stem cell culture was the highest, and there was no significant difference in the expansion efficiency between the unfixed group and the control group. The purity of NK cells in the fixed group was the highest. The activation culture on day 0 had the highest amplification efficiency and purity, and there was no significant difference in cell purity between activation culture and the 2 activation cultures on day 0 and 5, but the expansion efficiency of NK cells decreased significantly after 2 activation cultures. The killing activity of the stem cell group on K562 tumor cells was significantly better than that of the control group.  Therefore, gene-edited mesenchymal stem cells can improve the in vitro expansion efficiency of NK cells derived from peripheral blood,increase the purity of flow cytometry results, promote the killing activity of NK cell on tumor. The cost of this protocol is lower in addition to being safer and more effective. 
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  IL-21 regulates patient peripheral blood Treg in HBeAg-positive chronic hepatitis B

  CAI Yun, ZHOU Xin, PAN Liang, ZHAO Kai

  2025, 45(3): 291-296.

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  To explore the role of IL-21 in regulating the proportion of Treg and expression of key proteins in peripheral blood in the hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB), 45 HBeAg-positive CHB patients and 15 healthy controls (HC) were recruited. The biomarkers of hepatitis B, alanine transaminase (ALT), and load of HBV DNA were measured. PBMC isolated from CHB patients and HC were divided into IL-21 treated group and untreated group. The frequency of Treg was detected by flow cytometry and the mRNA expression levels of forkhead box protein 3 (Foxp3), IL-10 and TGF-β were detected by qRT-PCR. The expressions of IL-10 and TGF-β in the supernatant were measured by ELISA and the expressions of STAT3 and phosphorylated STAT3 (p-STAT3) were tested by Western blotting. The results showed that before IL-21 treatment, Treg proportion, Foxp3 mRNA, IL-10 mRNA, and IL-10 protein expression levels in CHB group were significantly increased（P<0.01）, while the expression levels of TGF-β mRNA and TGF-β protein were significantly decreased compared to those of the HC group（P<0.001）. Upon IL-21 treatment, Treg proportion, Foxp3 mRNA, TGF-β mRNA and TGF-β protein expression levels in CHB group and HC group were significantly lower (P<0.05), whereas IL-10 mRNA and IL-10 protein expression levels were significantly higher than those before treatment（P<0.05）. In addition, upon IL-21 treatment, the expressions of STAT3 and p-STAT3 in HC group and CHB group were significantly increased (P<0.05). Taken together, IL-21 may inhibit proliferation of Treg and secretion of TGF-β through activating STAT3 signaling pathway. Subsequently, the decrease in the number and function of Treg weakens the inhibitory effect of Treg on related effector cells, which related to the pathogenesis of CHB.
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  Alpinetin inhibits STING/TBK1/IRF3 pathway to improve intestinal barrier damage in sepsis rats

  CHEN Li, WANG Bochao, GAN Yingqi, HE Xiaoyu, TAN Zhijun, WANG Dongqiang

  2025, 45(3): 297-303.

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  The aim of the study was to investigate the effect of alpinetin on intestinal barrier damage in septic rats through regulating the stimulator of interferon gene (STING)/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3) signaling pathway. Rats were randomly divided into the sepsis group, the alpinetin group, the STING agonist (ADU-S100) group, the alpinetin+ADU-S100 group, and the blank control group, with 18 rats per group. Except the control group, sepsis model was established by cecal ligation and perforation procedure. After successful modeling, corresponding drugs were given once a day for 2 w. The serum level of fluorescein isothiocyanate FITC-glucan in each group was detected. H-E staining was used to evaluate the histopathological injury of small intestine. The expression of zonula occluden 1 (ZO-1) and Occludin in the small intestine was detected by immunohistochemical staining. Mean fluorescence intensity (MFI) of CD86 and CD206 in small intestine tissues was detected by immunofluorescence staining. The levels of TNF-α, IL-6, and IL-10 in the small intestine were detected by ELISA. Western blotting was used to detect the protein levels of STING, p-TBK1, and p-IRF3 in small intestine tissues. The results showed that compared to those of the control group, serum FITC-glucan level, small intestine mucosal Chiu score, CD86 MFI, TNF-α, IL-6 levels and STING, p-TBK1, p-IRF3 protein expressions in small intestinal tissues of sepsis rats were all increased, while the numbers of ZO-1 and Occludin positive cells, CD206 MFI, and IL-10 levels in the small intestine were significantly decreased (all with P<0.001). Compared to those of the sepsis group, serum FITC-glucan level, small intestine mucosal Chiu score, CD86 MFI, TNF-α, IL-6 levels, and STING, p-TBK1, p-IRF3 protein expressions in small intestinal tissues of the alpinetin group were all decreased, while the numbers of ZO-1 and Occludin positive cells in the small intestine, and the levels of CD206 MFI and IL-10 were increased (all with P<0.001). The dynamic trend of the above indexes in ADU-S100 group was opposite to those in the alpinetin group (all with P<0.001). ADU-S100 partially reversed the improvement of intestinal barrier damage in medicated sepsis rats (all with P<0.001). Therefore, the underlying mechanism of alpinetin in improving intestinal barrier damage in sepsis rats is closely associated with its inhibition of the STING/TBK1/IRF3 pathway.
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  The effect of c-Myc on the differentiation, proliferation, and apoptosis of mice T cells

  TENG Xiaoyan, WANG Weixiao, SUI Jun, WANG Biao, HUANG Jing

  2025, 45(3): 304-310.

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  To investigate the effect of the different expression levels of  c-Myc  on the differentiation, proliferation, and apoptosis of OT-Ⅰ T cells, OT-Ⅰ T cells were transfected with MSGV c-Myc GFP retrovirus. OT-Ⅰ T cells with high expression of GFP (c-Mychigh group) or low expression of GFP (c-Myclow group) were selected by FACS. qRT-PCR and Western blotting were used to detect the expression of c-Myc in OT-Ⅰ T cells. The expression levels of CD44 and CD62L on the surface of OT-Ⅰ T cells and the expression levels of cytokines IL-2 and Granzyme B (GrB) in OT-Ⅰ T cells were detected by flow cytometry. Western blotting was used to detect the expression levels of proliferating cell nuclear antigen (PCNA) and the proteins that were related to apoptosis in OT-Ⅰ T cells. The proliferation rate of OT-Ⅰ T cells was detected by cell counting. The results showed that high expression of c-Myc promoted T cell differentiation into memory T cells and the proliferation rate of OT-Ⅰ T cells, and enhanced the expression of PCNA protein. Furthermore, higher expression of c-Myc up-regulated the expression of anti-apoptotic protein B cell lymphoma2 (Bcl-2), inhibited the expressions of apoptotic protein Bcl-2-associated X protein (Bax), and the activation and degradation of Caspase-3. In conclusion, the increased expression of c-Myc in OT-Ⅰ T cells plays a role in promoting proliferation and inhibiting apoptosis of OT-I T cells.
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  Cryptotanshinone regulates the inflammatory response in neonatal necrotizing enterocolitis rats by the JAK2/STAT3 signaling pathway

  WANG Jing, GUAN Junyan

  2025, 45(3): 311-316.

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  This study aims to investigate the effect of cryptotanshinone (CRY) on the inflammatory response in neonatal rats with necrotizing enterocolitis (NEC) by the JAK2/STAT3 signaling pathway. Ten newborn SD rats were randomly selected as the negative control (NC) group, while the remaining rats were subjected to cold stimulation under hypoxic conditions to establish the NEC model. The successfully modeled rats were randomly divided into the NEC group, the CRY group (7 mg/kg CRY), the JAK2/STAT3 signaling pathway activator coumermycin A1 (C-A1) treatment group (100 μg/kg C-A1), and the CRY+C-A1 group (7 mg/kg CRY+100 μg/kg C-A1), with 10 rats in each group. The NC group and NEC group were given equal amounts of physiological saline, once a day for 2 consecutive weeks. The levels of inflammatory factors and oxidative stress indicators were measured by ELISA. The pathological changes of ileum tissue were detected by H-E staining. Apoptosis of ileal cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. The expressions of JAK2/STAT3 pathway-related proteins were detected by Western blotting. The results showed that compared to those of the NC group, the H-E inflammatory score, levels of IL-1β, IL-6, TNF-α, monocyte chemoattractant protein 1 (MCP-1), malondialdehyde (MDA), apoptosis rate, phosphorylated JAK2 (p-JAK2)/JAK2, phosphorylated STAT3 (p-STAT3)/STAT3 protein levels all significantly increased in the NEC group (P<0.05). On the contrary, the superoxide dismutase (SOD) level significantly decreased (P<0.05). Compared to that of the NEC group, the severity of intestinal tissue lesions in the CRY group decreased, along with the H-E inflammatory score, levels of IL-1β, IL-6, TNF-α, MCP-1, MDA, cell apoptosis rate, p-JAK2/JAK2, p-STAT3/STAT3 protein levels all reduced significantly (P<0.05), while the SOD level significantly increased (P<0.05). In the C-A1 group, the change patterns of above indexes were opposite to those of the CRY group, suggesting that C-A1 eliminated the improvement effect of CRY on NEC rats. Therefore, CRY may improve the inflammatory response in NEC rats by down-regulating the JAK2/STAT3 signaling pathway. 
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  The role of CCL20/CCR6 in unexplained recurrent spontaneous abortion

  YANG Li, XU Minqin, DONG Dantong, ZHU Qing, WANG Yulu, ZHANG Hong

  2025, 45(3): 317-323.

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  This study aims to explore the role of chemokine C-C motif ligand 20 (CCL20)/C-C chemokine receptor type 6 (CCR6) in unexplained recurrent spontaneous abortion (URSA). Non-pregnant URSA patients (n=22) and early-pregnant URSA patients (n=62) were enrolled as study group, while non-pregnant healthy women (n=30) and early-pregnant healthy women (n=42) were enrolled as control group. CCL20 in peripheral blood were detected by ELISA, and the pregnancy outcomes were followed up. The decidua tissues of URSA (n=36) were collected as the URSA group, and those from normal early pregnant women (n=29) who voluntarily terminated pregnancy during the same period served as the normal group. qRT-PCR was conducted to compare the mRNA expression levels of CCL20 and CCR6 in decidua between the 2 groups. Western blotting was used to compare the protein expressions of CCL20 and CCR6 in decidua between the 2 groups. The expression and localization of CCR6⁺Th17 cells in decidua of the 2 groups were compared by immunofluorescence staining. The results showed that the level of peripheral blood CCL20 in normal early pregnant women was higher than that in URSA early pregnant patients(P<0.05). The mRNA and protein expression levels of CCL20 and CCR6 in decidua of the URSA group were higher than those of the normal group (P<0.05). The number of CCR6⁺Th17 cells in the decidua of URSA patients was higher than that of the normal group. Together, this study suggests that changes in levels of peripheral blood CCL20 have little correlation with pregnancy outcomes. However, at the maternal-fetal interface, CCL20 may chemotactically induce CCR6⁺Th17 cells to migrate and accumulate at the maternal-fetal interface in early pregnancy of URSA patients, causing abortion.
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  The role of adipose tissue-resident immune cells on the pathogenesis of obesity

  ZHEN Lan, HUANG Qing, ZHAO Guilin, ZHAO Ruzhou, WEI Congwen, WU Feixiang

  2025, 45(3): 324-327.

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  The population of obese people is increasing, and obesity has become an important public health problem for human society. The mechanism of obesity development is complicated, and the immune-metabolic network plays a vital role in the process of obesity pathogenesis, which has become a focus of obesity research. A variety of immune cells reside in the adipose tissue and exert specific immune and metabolic modulations, which are essential for the routine function of adipose tissue. In-deep understanding of the role of adipose tissue-resident immune cells in the development of obesity can provide new research directions and potential efficient targets for the prevention and treatment of obesity.
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  Research progress of mucin-type O-glycosylation and ulcerative colitis

  YANG Xinke, ZHOU Yongxue, YANG Mingjie, YAN Shuguang

  2025, 45(3): 328-333.

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  Ulcerative colitis (UC) is an inflammatory bowel disease based on the pathological damage of the colon mucus barrier due to a variety of internal and external factors. The disorders of local immune system and intestinal flora are important factors leading to the damage of intestinal mucus barrier. Mucins, a major component of the intestinal mucus layer, are produced by goblet cells and may be post-translational modified by O-glycosylation. Mucin-type O-glycosylation not only ensures the integrity of the mucus layer, but also participates in the occurrence and development of UC by regulating the immune system and intestinal flora. This review summarizes the main mechanism of mucin-type O-glycosylation in the pathogenesis of UC, aiming to provide new ideas for prevention and treatment of UC.
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  Research progress on the association between gut microbiota and triple-negative breast cancer immunotherapy

  LIU Qinguo, CHEN Qishuai, MA Zhijun

  2025, 45(3): 334-338.

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  Triple-negative breast cancer (TNBC) is highly malignant and prone to recurrence and metastasis, which currently lacks effective treatment except surgery and chemotherapy. The emergence of immunotherapy, mainly immune checkpoint inhibitor (ICI), has provided a new strategy for TNBC treatment. Nevertheless, some patient population still can not benefit from immunotherapy. Recent studies suggest that gut microbiota and their metabolites may influence the immune efficacy of ICI on TNBC by regulating the tumor immune microenvironment (TIME). This review discusses the recent progress on the connection between gut microbiota and TNBC immunotherapy, aiming to provide new ideas for immunotherapy of this disease.
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  Research progress on the effect of IL-18 and IL-37 in mast cell activation in inflammatory diseases

  WANG Junling, ZHAN Mengmeng, ZHAO Zhuo, ZHANG Zhaolong, ZHENG Hui, ZHAO Congyi, ZHAO Danyang, ZHANG Yijie, QIN Bingyu

  2025, 45(3): 339-343.

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  IL-18 and IL-37 are cytokines of the IL-1 family, which play a biological antagonistic role in the inflammatory response by binding IL-18Rα. Mast cell (MC), the central effector cell in inflammation, is capable of inducing inflammatory response by secreting an array of inflammatory mediators, chemokines, and cytokines upon activation. Hence, a comprehensive understanding of the actions of IL-18 and IL-37 on MC activation is imperative to the diagnosis and treatment of MC-related inflammatory diseases, as well as the development of IL-18- and IL-37-related biological agents. The review focuses on the effects of IL-18 and IL-37 on MC activation in order to provide new directions for research on IL-18, IL-37, and MC.
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  Immunomodulatory effect and mechanism of placental mesenchymal stem cells

  YOU Lijuan, ZHU Ziwen, XU Guiling, QIAO Jing

  2025, 45(3): 344-349.

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  The placenta obtained from a full-term delivery provides abundant tissue source for obtaining high-quality mesenchymal stromal cells (MSC). These cells are recognized for their robust regenerative capacity and immunosuppressive effects. Because placenta MSC have immunosuppressive effects and are easily obtained from theobstetrics and gynecology department without raising ethical concerns, they are considered to be the most promising transplantation cells and are widely used in the treatment of anti-graft host rejection, autoimmune diseases and non-immune diseases with inflammatory components.This review summarizes the characteristics and immune regulatory mechanisms of placental mesenchymal stem cells (PMSC), aiming to present new ideas for the clinical utilization of PMSC.
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  Research progress on the modulation of macrophage polarization in chronic skin wound healing

  YANG Qiuxia, TAO Hongxia, PEI Juhong, LYU Lin, WEI Yuting, HAN Lin

  2025, 45(3): 350-354.

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  Chronic skin wound healing is one of the challenges in the field of repairing. Macrophages play an important modulatoryrole in wound healing and they may polarize to M1 or M2 phenotypes in different microenvironments and upon various stimuli. Dysregulation of the macrophage phenotypes is a vital factor in chronic skin wound healing, and correction of the macrophage phenotypes can promote wound healing. This review summarizesthe origin of skin macrophages, the polarization of macrophages, the mechanism and strategy to regulate macrophages polarization and promote skin chronic wound healing in order to provide evidence for skin chronic wound healing.
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  Expression, function, and clinical value of the IL-33/ST2 axis in central nervous system and glioma

  HE Jing

  2025, 45(3): 355-359.

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  Glioma is the most common primary brain tumor. Traditional treatments have limitations including poor therapeutic effect and  prognosis. Therefore, it is important to search for key signaling molecules and effective biomarkers for the diagnosis and treatment of glioma. IL-33 plays an important role in both type 1 and type 2 immune responses, participates in synaptic formation, maturation, and remodeling, and maintains synaptic homeostasis. In glioma tissue specimens and animal models, the expressions of IL-33 and its receptor suppression of tumorigenicity 2 (ST2) were significantly increased. IL-33 enhances glioma proliferation and migration by mechanisms including the regulation of signaling pathways such as the IL-33/ST2/NF-κB and shaping the tumor microenvironment through the competition of trans-membrane ST2(ST2L) and soluble ST2(sST2). IL-33/ST2 axis is a key axis linking the homeostasis of the nervous system and the immune system, which has potential diagnostic and prognostic value. IL-33 is expected to be combined with other treatment strategies to become a comprehensive sequential therapy for glioma. This review summarizes the immune mechanism and diagnostic applications of IL-33 and its receptor ST2 in glioma diseases. 
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  Regulation of m6A modification on the pathogenesis of ankylosing spondylitis

  XIA Yannan, HUANG Chuanbing, DU Shuhui, CHEN Xiaohan, XU Jiamin

  2025, 45(3): 360-364.

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  N6-methyladenosine (m6A) is an important epigenetic regulatory mechanism that participates in and regulates a variety of biological processes. In recent years, m6A methylation has been found to play an important role in the pathogenesis of ankylosing spondylitis (AS), a type of spondyloarthritis that mainly affects the spine and sacroiliac joints, resulting in pain, stiffness, and spinal ankylosis. The pathogenesis of AS is complex and involves a variety of factors, including genetics, infection, immunity, and environment. The pathogenesis of AS is complex and involves many factors, including genetics, infection, immunity, and environment, etc. Notably, m6A plays a regulatory role in all of these factors. In this review, we will discuss the pathogenesis of AS from the aspect of m6A-mediated genetic regulation.
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  Research progress of exosomes on pathogenesis, diagnosis, and treatment of primary Sjogren's syndrome

  REN Yuan, LI Xiaofang, CHEN Xiangni, HU Tao, ZHAO Jing, HAO Jianmei

  2025, 45(3): 365-370.

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  Exosomes are extracellular vesicles of 30-150 nm in diameter, which are mainly composed of proteins, DNA and RNA wrapped by phospholipid bilayers. They have become important mediators of intercellular immune regulation due to their high stability, low immunogenicity, low toxicity, long half-life and the ability to penetrate the blood-brain barrier. Current studies have shown that their intercellular communication function is involved in the structural and functional disruption of exocrine glands in the Sjogren's syndrome. This review summarizes the current research progress on the functions of exosomes in the immunomodulation, pathogenesis, diagnosis and treatment of the Sjogren's syndrome.
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  Research progress on the interaction between macrophages and aerobic glycolysis in hepatocellular carcinoma

  LIU Qinglin, CHEN Che, FAN Mengge, FAN Tingting, MA Xiaoxia, DAI Rui, LIU Fang

  2025, 45(3): 371-375.

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  Macrophages are the most abundant immune cells in liver cancer tissues, which can be polarized into pro-inflammatory and anti-tumor M1-type or anti-inflammatory and pro-tumor M2-type macrophages upon different stimuli. Macrophages have high plasticity and heterogeneity, and their functional phenotypes are closely related to the tumor microenvironment. Aerobic glycolysis is one of the most important metabolic features of tumor cells. Therefore, exploring the interaction between aerobic glycolysis and macrophages may provide a new therapeutic direction for the treatment of hepatocellular carcinoma and other diseases closely related to the tumor microenvironment. In this review, we focus on the effects of key metabolites of aerobic glycolysis on macrophages and macrophage-associated cytokines on aerobic glycolysis to introduce the interplay between them and summarize the key enzymes of aerobic glycolysis and the role of macrophages in hepatocellular carcinoma.
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  Study on the pleiotropy of ILC and related cytokines in cancer

  ZHANG Linguang, YIN Haijuan, ZHANG Rongye, DONG Tao

  2025, 45(3): 376-380.

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  ILC, a type of immune cells located in tissues that can rapidly respond to changes in the surrounding environment, has been the focus of research in recent years, and plays an irreplaceable role in the occurrence, progression and metastasis of tumors. This review summarizes the effect of different ILC subsets and their related cytokines in promoting or inhibiting the growth of different types of tumor through the interaction with the tumor microenvironment, which provides a more comprehensive understanding of the influence of ILC in tumors.