30 September 2025, Volume 45 Issue 5

  

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  Immune cells: key to thermogenesis and metabolic disorder regulation in adipose tissue

  WANG Kefan, LU Liming

  2025, 45(5): 493-501.

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  Obesity is the excessive accumulation of fat caused by the imbalance between energy intake and expenditure, which has become a global health issue. The metabolic homeostasis of adipose tissue plays a crucial role in the progression of obesity and has numerous impacts on systemic physiology. Studies have found that various immune cells and cytokines are involved in maintaining and regulating the metabolic homeostasis of adipose tissue, suggesting the significant potential of immune cells in alleviating obesity and insulin resistance (IR). From the perspectives of innate and adaptive immunity, this review discusses the progress on the role of immune cells in thermogenesis and metabolic functions of adipose tissue and further explores the therapeutic potential of the immune system in obesity and related metabolic disorders.
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  Selective involvement of the STAT family transcription factors in regulating the differentiation of helper T cells

  LI Xiyue, DONG Chen, ZHONG Yi

  2025, 45(5): 502-510.

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  The aim of this study is to explore the regulatory features, co-regulatory roles and effects on the epigenome of the STAT family proteins and the master transcription factors of the Th1, Th2, and Th17 subtypes, including the T-box expressed in T cell (T-bet), GATA binding protein 3 (GATA3), and retinoic acid receptor-related orphan receptor γt (RORγt) in Th differentiation. Assay for transposase-accessible chromatin using sequencing (ATAC-seq) data of different T cell differentiation stages and chromatin immunoprecipitation sequencing (ChIP-seq) data of transcription factors were obtained and integrated from the GEO database. The co-localization, the genomic distribution of the transcription factors, and the chromatin accessibility changes during differentiation and functions of regulated genes were analyzed. The results showed that the transcription factor STAT2 was the main STAT family transcription factor involved in the maintenance of Th0 chromatin characteristics. STAT4 was widely co-localized with T-bet and regulated Th1 activation. The master regulator GATA3 and the co-factor STAT6 preferentially bound to non-promoter cis-elements thereby directing Th2 differentiation. RORγt, the master transcription factor, enhanced the binding strength of STAT3 and STAT5 in a distinctive manner independent of altered chromatin accessibility, co-regulating Th17-specific differentiation. This study suggests that STAT family transcription factors selectively participate in and differentially regulate Th differentiation.
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  Investigation of the effect of total alkaloids of Strychni Semen on the apoptosis of synovial cells in rheumatoid arthritis rats via the Wnt3a/β-catenin pathway

  ZHANG Guanghui, WEI Qin, LI Kun, SU Liyun, RUAN Wensi

  2025, 45(5): 511-518.

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  To analyze the effect of total alkaloids of Strychni Semen on the apoptosis of synovial cell and on the Wnt3a/β-catenin signaling pathway in rheumatoid arthritis (RA) rat, a total of 40 SPF-level SD rats were prepared, with 10 for the control group and 30 for the RA model group. Twenty-seven rats in total were successfully modeled and were divided into the model group, the total alkaloids of Strychni Semen group, and the total alkaloids of Strychni Semen+Wnt3a agonist group, with 9 rats per group. Histopathological features, toe-swelling degree, arthritis index, immune organ index, synovial cell apoptosis rate, inflammatory factors concentration, and Wnt3a/β-catenin pathway gene transcription and expression were measured in each group. The results showed that the synovial tissue structure of the control group was normal without hyperplasia or inflammatory infiltration. In the model group, the synovial tissue shape was rough, with hyperplasia and infiltration of inflammatory cells. The synovial hyperplasia and inflammatory infiltration were alleviated in the total alkaloids of Strychni Semen and the total alkaloids of Strychni Semen+Wnt3a agonist groups. Compared to those of the control group, toe swelling, arthritis index, thymus index, spleen index, IL-6, IL-17, IL-1β, and TNF-α levels, Wnt3a, β-catenin mRNA and protein expression levels increased in the model group, while the apoptosis rate of synovial cells decreased. Compared to those of the model group, toe swelling, arthritis index, thymus index, spleen index, IL-6, IL-17, IL-1β, and TNF-α levels, Wnt3a, β-catenin mRNA and protein expression in the total alkaloids of Strychni Semen group were decreased, while the apoptosis rate was increased. Compared to the total alkaloids of Strychni Semen group, the total alkaloids of Strychni Semen+Wnt3a activator group showed increased toe swelling, arthritis index, thymus index, spleen index, IL-6, IL-17, IL-1β, and TNF-α concentrations, Wnt3a, β-catenin mRNA and protein expression levels and decreased apoptosis rate of synovial cells (all above with P＜0.05). In conclusion, total alkaloids of Strychni Semen can inhibit intraarticular inflammation and promote synovial cell apoptosis in RA rats by modulating the Wnt3a/β-catenin signaling pathway.
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  PAD4 negatively regulates the TLR4/NF-κB signal pathway to alleviate adipose tissue inflammation

  Zhang Xinyue, Cheng Yi, Zheng Wenxiang, Zhai Qiaoli, Xiang Xinxin

  2025, 45(5): 519-530.

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  The purpose of this study is to explore the role and mechanism of peptidyl arginine deimidase type 4 (PAD4) in inflammatory adipose tissue. The subcutaneous and visceral adipose tissues of db/db (type 2 diabetes mellitus [T2DM] group), db/m (T2DM control group), ob/ob (obese group) and ob/c(obese control group) were extracted, and the expression of PAD4 in subcutaneous and visceral adipose tissue of T2DM and obese mice was detected by immunohistochemistry. Wild-type mouse primary peritoneal macrophages and mouse macrophage cell line RAW264.7 were stimulated with LPS, the expressions of PAD4, inflammatory factors TNF-α and IL-6, the activation of NF-κB signal pathway in the 2 types of cells were detected by qRT-PCR and Western blotting, respectively. The results showed that compared to those of the db/m and ob/c groups, the expression of PAD4 in subcutaneous and visceral adipose tissue, primary peritoneal macrophages and RAW264.7 cells stimulated by LPS in db/db and ob/ob groups were all decreased, while the expressions of inflammatory factors TNF-α and IL-6 increased significantly.Meanwhile, the TLR4/NF-κB signal pathway was activated. This study shows that the expression of PAD4 is decreased in subcutaneous and visceral adipose tissue in inflammatory state (T2DM and obesity) and is negatively correlated with the activation of the TLR4/NF-κB signal pathway.
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  Preliminary study on the inhibition of sST2 on cardiac fibroblast pyroptosis and myocardial fibrosis in a viral myocarditis mouse model

  CUI Congcong, SITU Qiuchen, LYU Hongxiang

  2025, 45(5): 531-538.

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  This study was designed to explore the potential relationship between myocardial fibrosis and the pyroptosis of mouse cardiac fibroblast (MCF) regulated by soluble growth stimulation expressed gene 2 (sST2). A mouse model of viral induced myocarditis (VMC) was established, and mice were divided into the VMC group and the VMC+ST2 antibody group in addition to a control group. Mice were sacrificed on the 7th day and cardiac inflammatory infiltration was observed by H-E staining and collagen deposition was observed by Masson staining. Western blotting was conducted to detect the expressions of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), IL-1β, cleaved caspase-1, GSDMD-N, and activation markers collagen Ⅰ/Ⅲ and α-SMA after sST2 treatment of MCF. After MCC950 pretreatment, the expressions of NLRP3, IL-1β, cleaved caspase-1, GSDMD-N, and activation markers collagen-Ⅰ/Ⅲ and α-SMA were detected. The mRNA expressions of IL-1β, IL-18, NLRP3, collagen-Ⅰ/Ⅲ and α-SMA after MCC950 pretreatment were detected by qRT-PCR. The results showed that the expressions of NLRP3, IL-1β, IL-18, cleaved caspase-1, and GSDMD-N were significantly increased after sST2  treatment of MCF. Activation indexes collagen-Ⅰ/Ⅲ and α-SMA were up-regulated. After MCC950 pretreatment, the expressions of NLRP3, IL-1β, IL-18, cleaved caspase-1, and GSDMD-N were down-regulated. The activation indexes of collagen-I/III and α-SMA were significantly reduced. In vivo ST2 blockage caused reduced myocardial inflammatory infiltration and collagen deposition. In conclusion, sST2 activates NLRP3 inflammasome to induce MCF pyroptosis and promote myocardial fibrosis.
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  Neuroprotective effects on Parkinson's disease cell model by Huanglian Jiedu Tang via antagonizing the NLRP3 inflammasome pathway

  CHEN Juan, HU Qi, LI Guiyou, LI Hui, LIU Zhou, LIU Daozhong, JIANG Jinlin, YUAN Lin

  2025, 45(5): 539-548.

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  To explore the neuroprotective effect of Huanglian Jiedu Tang on Parkinson's disease (PD) cell model by the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome pathway, a PD cell model was established by adding 6-hydroxydopamine (6-OHDA) to human neuroblastoma cells (SH-SY5Y). The serum of rats gavaged with Huanglian Jiedu Tang was obtained and cells were treated with different concentrations of drug drug-containing serum or blank serum. The concentration of drug-containing serum was screened using the CCK-8 method. ELISA was used to detect the content of lactate dehydrogenase (LDH) in the cell supernatant. Flow cytometry was used to detect cell apoptosis and the expression of reactive oxygen species (ROS). β-galactosidase staining was used to detect cellular aging. Immunofluorescence assay was used to detect the expression of α-synuclein (α-Syn) and phosphorylated α-Synuclein (p-α-Syn). Western blotting was used to detect the protein expressions of NLRP3, caspase-1 and its precursors pro-Caspase-1, α-Syn, IL-1β and its precursor pro-IL-1β, and IL-18 in each group. Compared with the model group, the low, medium, and high dose Huanglian Jiedu Tang groups showed reduction of LDH content, cell apoptosis rate, and the β-galactosidase increase caused by PD. In contrast, the treatments inhibited the protein expressions of NLRP3, caspase-1, α-Syn, p-α-Syn, IL-1β and IL-18. In summary, Huanglian Jiedu Tang inhibits the inflammation damage of SH-SY5Y cells in PD model induced by 6-OHDA, possibly by regulating the NLRP3 inflammasome pathway, which provides a theoretical basis for the treatment of PD with Huanglian Jiedu Tang.
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  Kaempferol relieves nasal mucosal injury in allergic rhinitis rats via the TLR4/NF-κB/TNF-α signaling pathway

  WANG Yongbao, LI Aijun, HAN Jiancun, ZHANG Haidong

  2025, 45(5): 549-554.

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  To investigate the effect of kaempferol on nasal mucosal injury in allergic rhinitis (AR) rats via the TLR4/NF-κB/TNF-α signaling pathway, rat AR model was established. Subjects were randomly divided into the model group, the low-dose (50 mg/kg) kaempferol group, the high-dose (100 mg/kg) kaempferol group, and high-dose (100 mg/kg) kaempferol+LPS (0.4 mg/kg) group as well as the control group. Rhinitis symptoms in rats were observed and scored after drug intervention. H-E staining was applied to observe the pathological changes in rat nasal mucosal tissues. ELISA was used to detect the levels of IL-6, TNF-α in rat nasal lavage fluid (NLF) and of serum IgE. Western blotting was used to detect the protein expressions of TLR4, NF-κB, and TNF-α in nasal mucosal tissues. The results showed that the rhinitis symptom score of the model group was significantly higher than that of the control group (P＜0.05). In addition, pathological changes in the nasal mucosal tissue of the model group were obvious. The levels of IL-6, TNF-α in NLF, IgE in serum, and the protein expressions of TLR4, NF-κB, and TNF-α in nasal mucosal tissues were also significantly increased (all with P＜0.05). Compared to the model group, the medicated rats showed decreased rhinitis symptom scores (both P＜0.05) and alleviated pathological injury. The levels of IL-6, TNF-α in NLF, IgE in serum, and the protein expressions of TLR4, NF-κB, and TNF-α in nasal mucosal tissues were also all decreased. These observations were particularly evident in the high-dose kaempferol group (all with P＜0.05). In contrast, LPS, the TLR4 activator, reversed the effects of kaempferol on AR rats (all with P＜0.05). In summary, kaempferol inhibits the TLR4/NF-κB/TNF-α signaling pathway and alleviates the pathological injury and inflammatory responses of nasal mucosa in AR rats, which in turn improves the disease symptoms.
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  The therapeutic effect of acacetin on rats with depression

  Li Zhuo, Meng Xiangyu, Zhang Jinhui, Feng Na, Shi Cuicui, Zhang Bin

  2025, 45(5): 555-561.

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  The aim of this study was to investigate the therapeutic effect of acacetin on depressed rats and its regulation on the HIF-1α/NLRP3 signaling pathway. A rat model of depression was established, and rats were divided into the model group, the acacia low-dose group, the acacia high-dose group and the acacia high-dose + pathway activator group (acacia high-dose+BMS-986299 group), with 12 rats in each group, in addition to a control group. After the treatment was completed, the sugar water preference, the mine field experiment, and the forced exercise experiment were performed, respectively. ELISA was used to detect levels of inflammatory and oxidative stress factors. H-E and Nissl staining were used to observe the histopathological morphology and neuronal number of hippocampus. Western blotting was used to detect the expression of proteins related to the HIF-1α/NLRP3 signaling pathway. Compared to those of the control group, the hippocampal tissue structure of the model group was damaged, the pyramidal cell arrangement was disordered, the nuclear condensation phenomenon was obvious, and the numbers of Nissl bodies and neurons decreased. In the meantime, the sugar water preference rate, voluntary activity score, and the level of CAT were decreased, whereas the immobility time of forced swimming, the levels of IL-6, IL-β, TNF-α, reactive oxygen species (ROS), malondialdehyde (MDA), and the expression of HIF-1α, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1 were increased (P<0.05). Compared to those of the model group, the hippocampal tissue structure of the acacia low-dose and high-dose groups was relatively normal, and the pyramidal cells were relatively intact and well arranged, the nuclear condensation phenomenon was reduced, and the numbers of Nissl bodies and neurons increased. Consistently, the sugar water preference rate, voluntary activity score, and the level of CAT increased, while the immobility time of forced swimming, the levels of IL-6, IL-β, TNF-α, ROS, MDA, and the expression of HIF-1α, NLRP3, ASC and caspase-1 decreased (P<0.05). Compared to those of the acacia high-dose group, the hippocampal tissue structure damage and pyramidal cell arrangement disorder were aggravated in the acacia high-dose +BMS-986299 group. The nuclear condensation phenomenon was intensified and the numbers of Nissl bodies and neurons decreased. The sugar water preference rate, voluntary activity score, and the level of CAT decreased, while the immobility time of forced swimming, the levels of IL-6, IL-β, TNF-α, ROS, MDA, and the expression of HIF-1α, NLRP3, ASC and caspase-1 were increased (P<0.05). Together, these findings demonstrate that acacetin has therapeutic effect on depression rats, and underlying mechanism is related to the inhibition of the HIF-1α/NLRP3 signaling pathway.
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  Correlation study of peripheral blood free CD44 and CD69 levels during early pregnancy with the preeclampsia and neonatal outcomes

  WANG Ning, YANG Lifan, ZHAO Weihua, KE Weilin

  2025, 45(5): 562-569.

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  The retrospective study aimed to investigate the correlation between the expression levels of free CD44 and CD69 in peripheral blood during early pregnancy and the occurrence of preeclampsia, in addition to evaluate the correlation with the disease severity and neonatal  outcome. One hundred pregnant women cases  with preeclampsia admitted to The First Affiliated Hospital of Shenzhen University (Shenzhen Second People's Hospital) from 1/1/2018 to 12/31/2023 were enrolled as the preeclampsia group, and 100 healthy pregnant women enrolled during the same time period were set as the control group. Clinical baseline data including age, body mass index (BMI), blood pressure, BMI at admission, blood pressure at admission, random urine protein quantification, gestation days, and birth weight of newborns were collected. The expression levels of free CD44 and CD69 in the peripheral blood  were detected by ELISA. The results showed that the levels of peripheral free CD44 and CD69 in the preeclampsia group were significantly lower than those of the control group (both P＜0.001). Multivariate Logistic regression analysis showed that, after controlling for potential confounding factors, CD44 and CD69 still showed independent impacts on the occurrence of preeclampsia (both P＜0.001). In addition, the levels of CD44 and CD69 significantly affected the severity of preeclampsia (all with P＜0.05). ROC curve analysis showed that the area under the curve (AUC) of either CD44 or CD69, and that of the combination of the two factors were all above 0.7, indicating their predictive value for preeclampsia, with combination of CD44 and CD69 being the best predictor (AUC=0.968, P＜0.001). In terms of neonatal outcomes, free CD44 and CD69 levels in peripheral blood during the first trimester were positively correlated with neonatal birth weight and gestation days (all with P＜0.05). In conclusion, the levels of free CD44 and CD69 in peripheral blood during early pregnancy can be used as a biomarker to predict the occurrence of preeclampsia, and may provide auxiliary information for evaluating the severity of preeclampsia and neonatal outcomes, as well as a reference for personalized clinical screening and prevention strategies.
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  IL-33 knockdown reduces airway inflammation in a mouse asthma model

  LIN Mali, SHENG Fang

  2025, 45(5): 570-577.

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  This study investigated the role of IL-33 knockdown in attenuating airway inflammation in a mouse asthma model, aiming to identify novel therapeutic targets for asthma. Bone marrow-derived mesenchymal stem cells (BMMSC) were isolated from mice and transduced with IL-33-silencing plasmids (si-IL-33-1^#, si-IL-33-2^#, si-IL-33-3^# and a scrambled control plasmid ) via lentiviral system. The efficiency of IL-33 knockdown was validated by qRT-PCR. An asthma mouse model was established using a combined sensitization and challenge protocol with ovalbumin (OVA). Mice were divided into 5 groups: the control group; the asthma model group; the BMMSC-treated group; the BMMSC+empty vector group and the BMMSC+IL-33 knockdown group. Pathological changes in lung tissues were assessed by H-E staining, Masson's trichrome staining, and immunohistochemistry (IHC). Serum levels of IL-33, IL-1β, and IL-6 were quantified using ELISA. The result showed that primary BMMSC exhibited adherent growth with spindle or polygonal morphology. Flow cytometry was used to measure the expressions of surface markers: CD90 positivity rate was 99.30%; CD29 positivity rate was 100.00%; while hematopoietic lineage markers CD45 and CD34 showed minimal positivity (0.34% and 1.24%, respectively). qRT-PCR demonstrated that the si-IL-33-3^# plasmid effectively silenced IL-33 expression in BMMSC, confirming that it was an optimal IL-33 knockdown construct. Histopathological analysis revealed the BMMSC+IL-33 knockdown group displayed minimal inflammatory cell infiltration in lung tissue, with intact bronchial epithelium. IHC staining showed that BMMSC+IL-33 knockdown group exhibited significantly reduced α-smooth muscle actin (α-SMA) and vascular endothelial growth factor B (VEGFB) relative expressions compared to those in the asthma model group and the BMMSC-treated group (P<0.05). ELISA analysis further confirmed the markedly decreased serum levels of IL-1β, IL-6, and IL-33 in the BMMSC+IL-33 knockdown group compared to either the model or the BMMSC-treated groups (P<0.05). Altogether, IL-33 knockdown attenuates inflammatory response in the asthma mouse model and thereby prevents the lung lesions associated with asthma. 
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  Experimental study on the isolation of ILC2 from mouse lung tissue using magnetic bead sorting method

  LI Xinrong, LI Yu, Chen Xi, HUANG Yue, SUI Wen, CHEN Yulan, Li Qihong, YANG Hao, YIN Man, LYU Zeyi

  2025, 45(5): 578-584.

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  This study aimed to develop the optimal enzymatic combination for single-cell suspension from mouse lung, and to explore the isolation and culture of the type 2 innate lymphoid cells (ILC2) using immunomagnetic bead separation and flow cytometry. 10 mice were divided into 4 groups for different enzymatic isolation methods, including collagenase Ⅳ, Lung Dissociation Kit, Liberase TM, and collagenase P+dispase Ⅱ, respectively. The most optimal enzymatic isolation method was chosen based on the ratio of living, CD45⁺ and c-kit⁺ cells. Immunomagnetic bead enrichment (EasySep Mouse ILC2 Enrichment Kit) and FACS were used to isolate ILC2 and flow cytometry was used to measure ILC2 homogeneity．Cells cultured in vitro were divided into 2 groups by treatment of IL-33 to evaluate its promoting effect on the in vitro culture of ILC2. Western blotting was used to detect the protein levels of GATA binding protein 3 （GATA-3）, IFN-γ, IL-5 and IL-13. The results indicated that the combination of collagenase P+dispase Ⅱ was the most suitable method for cell isolation of mouse lung with higher ratios of target cell and better cost-effectiveness. The percentage of ILC2 in the enriched fraction reached 2.14% compared to less than 1% before enrichment. The expressions of IFN-γ, IL-5, IL-33 with IL-33 stimulation were higher than those of the control（P<0.001). However, GATA-3 expression showed no statistical significance between the 2 groups（P>0.05). In conclusion，collagenase P+Dispase Ⅱ is a feasible enzymatic digestion protocol for mouse lung tissue. The magnetic cell sorting system could be a rapid and efficient method for ILC2 isolation and future cultivation. In addition, IL-33 can enhance the viability of ILC2 in vitro and stimulate the expression of downstream cytokines. 
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  IL-6 promotes the occurrence and development of diffuse large B-cell lymphoma by regulating the JAK/STAT3 signaling pathway

  ZHAO Mingzhe, WANG Lili

  2025, 45(5): 585-592.

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  This study aimed to investigate the role of IL-6 in diffuse large B-cell lymphoma (DLBCL) and the role of IL-6 on cell apoptosis, proliferation, invasion and migration via the JAK/STAT3 signaling pathway. OCI-LY8 cell line was used as a DCBCL model and drug intervention of IL-6 or STAT3 gene silencing were used to assess the effect of IL-6 and STAT3 on OCI-LY8 cells. Cell viability was detected by CCK8 assay and apoptosis rate was determined by flow cytometry to study the effect of IL-6 on the proliferation and apoptosis of DLBCL cells. Transwell assay and scratch assay were used to detect cell invasion and migration capacity and elucidate the effect of different IL-6 concentrations on DLBCL migration. The expressions of JAK, STAT3 and the downstream apoptosis-related B cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and survivin proteins were detected by Western blotting. Western blotting showed that IL-6 up-regulated anti-apoptotic proteins Bcl-2 and survivin, and downregulated pro-apoptotic protein Bax by activating the JAK/STAT3 pathway, thereby inhibiting OCI-LY8 apoptosis. IL-6 could also enhance the invasion and migration of OCI-LY8 by activating STAT3. The effect of IL-6 was reversed upon IL-6 inhibitor LMT-28 treatment or STAT3 silencing. IL-6 enhanced the invasion and migration capacity of OCI-LY8 DLBCL cells by activating the JAK/STAT3 signaling pathway, as well as increasing their anti-apoptosis ability. Together, these findings reveal that IL-6 promotes DLBCL development via the JAK/STAT3 pathway, which provides a new potential target and theoretical basis for DLBCL treatment.
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  TRIM22 inhibits the directed migration of HIV-1 p55 to cell membrane through a proteasome-dependent pathway

  Zhang Ziyi, An Xinye, Wang Xiao, Sun Dakang

  2025, 45(5): 593-599.

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  This study aimed to investigate the co-localization of tripartite motif protein 22 (TRIM22) and human immunodeficiency virus-1 (HIV-1) p55, and understand its effect and mechanism on the directional migration of p55 toward cell membrane at single-cell level. pEGFP-N3-p55 and/or pDsRed1-N1-TRIM22 expression vectors were transfected into HEK293T cells, and confocal microscopy was used to observe the distribution pattern of p55-EGFP or TRIM22-DsRed1 protein. Next, pEGFP-N3-p55 and pDsRed1-N1-TTRIM22 expression vectors were co-transfected into HEK293T cells to observe the co-localization of TRIM22 and p55, and the effect of TRIM22 on the directional migration of p55-EGFP to cell membrane. Finally, proteasome inhibitor MG132 was administrated to observe the change of inhibited migration to the cell membrane of p55-EGFP by TRIM22. Confocal microscopy detected that the overexpression of p55-EGFP in HEK293T cells selectively migrated to cell membrane, and the overexpression of TRIM22-DsRed1 could be distributed in the cytoplasm or nucleus. Co-expression of p55-EGFP and TRIM22-DsRed1 in HEK293T cells led to their co-localization. Interestingly, TRIM22 can significantly inhibit the directional migration of p55 to cell membrane. The application of proteasome inhibitor MG132 can weaken the inhibitory effect of TRIM22 on the directional  migration of p55-EGFP protein to cell membrane. Taken together, when p55-EGFP and TRIM22-DsRed1 co-exist in HEK293T cells, they co-localize and TRIM22 inhibits the directional migration of p55 to the cell membrane in a proteasome-dependent manner. 
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  Autoantibody profiling in systemic lupus erythematosus patients

  SHEN Fangfang, WANG Qiong, WU lingqin, JIN Yingying, CHEN Tongxin

  2025, 45(5): 600-606.

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  The aim of this study is to understand the distribution of autoantibodies in systemic lupus erythematosus (SLE) patients and explore the role of SLE autoantibodies in organ function. Seventy-six newly diagnosed SLE patients admitted to the Second Hospital of Jiaxing  from January 2018 to December 2023 were selected. Indirect immunofluorescence was used to detect the autoantibodies index, and the data were analyzed. The results showed that most SLE patients suffered from arthritis (55.26%) and rash (52.63%). The positive rate of antinuclear antibody (ANA) was 100.00%, and among them the most common was the anti-Sjogren's syndrome A (SSA) antibody. Multiple autoantibodies in the vast majority of patients were positive (97.37%). The positive rate of anti-dsDNA antibody was the highest in the adolescent group (66.67%), but the lowest in the elderly group (33.33%). The positive rate of anti-dsDNA antibody in lupus nephritis (LN) was 76.47%. The positive rate of anti-Sm antibody was the highest in Raynaud＇s phenomenon and alopecia patients (33.33% and 50.00% respectively). The positive rate of anti-histone antibody (AHA) in vasculitis and LN patients was 75.00% and 58.82%, respectively. This study suggests that the clinical manifestations of SLE are different and highly heterogeneous, and multiple autoantibodies are correlated with organ involvement, clinical manifestations and age.
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  Cloning and bioinformatic analysis of mouse IL-36Ra gene

  CHENG Peng, LI Chunlin, CHEN Xudong, WANG Hehe, XIE Jiwei, WANG Yaowen

  2025, 45(5): 607-613.

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  This study aimed to clone mouse IL-36 receptor antagonist (mIL-36Ra) gene, analyze the secondary structures of IL-36Ra protein and its antigenic epitopes. Total RNA was extracted from mouse skin and the full-length cDNA sequence of mIL-36Ra was obtained by RT-PCR. Eukaryotic expression plasmid pcDNA3.1-mIL-36Ra/V5-His was constructed by ligating to pcDNA3.1/V5-His using restriction enzymes. The amino acid composition, physicochemical property and secondary structures were analyzed using ProtParam and SOPMA in Expasy. IEDB database online analytic tool was used to explore the hydrophilic, flexibility, accessibility and antigenicity of the protein to predict the B cell epitope. The restriction endonuclease analysis and DNA sequencing of the plasmid demonstrated that pcDNA3.1-mIL-36Ra/V5-His gene was correctly constructed and the sequence matched the sequence in GenBank 100%. Bioinformatics analysis showed that the secondary structure of mouse IL-36Ra protein mainly consisted of random coils (41.03%), beta-fold (28.21%), alpha-helix (19.23%) and beta-angle (11.54%). The most possible epitopes of IL-36Ra were located in or adjacent to amino acid residues 16-25,29-31,43-49,65-71 and 131-135. The study successfully cloned mIL-36Ra gene and completed further biological analysis to provide the experimental and theoretical basis for IL-36Ra protein expression, protein purification and monoclonal antibody development.
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  Anti-cytokine autoantibodies and infectious diseases: clinical phenotypes and treatment

  ZHU Xinyun, CAO Shan, CHEN Xiaoxiang

  2025, 45(5): 614-620.

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  Anti-cytokine autoantibodies (ACAA) exist in various infectious and immune-related diseases, and have gained increasing attention in refractory infectious diseases in recent years. The titer of neutralizing autoantibodies is closely related to the severity and prognosis of infectious diseases. Patients with high titers of antibodies often have more severe clinical symptoms, less satisfactory anti-infective benefits, higher risk of recurrence, and worse prognosis. The correlation between ACAA and clinical phenotypes reveals new mechanisms of complex opportunistic and refractory infections, which provide new treatment strategies for diseases. This review focuses on ACAA related infectious diseases, describing different clinical phenotypes, introducing current treatment measures, and finally proposing the clinical and basic research directions of infection immunity in the future.
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  Research progress and prospect of TIM family proteins in viral infection and ocular disease

  ZHANG Chengxiao, CHU Yiran, HU Kai

  2025, 45(5): 621-626.

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  T cell immunoglobulin and mucin domain (TIM) family proteins, as emerging immune regulatory factors, are transmembrane proteins that can recognize phosphatidylserine (PS) and other ligands. TIM family proteins are predominantly expressed in immune cells such as T cells, macrophages, and DCs, which significantly overlap with resident immune cells in normal ocular surfaces. Studies have shown that TIM family proteins play crucial roles in viral infection, particularly in the process of viral entry into host cells. This review will systematically summarize the research progress of TIM family proteins, with particular focus on the research status of TIM-1, TIM-3, and TIM-4 identified in human cells, in the context of viral infections and ocular diseases, and explore their potentials in future disease prevention and treatment.
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  Research progress on peripheral helper T cells in autoimmune diseases

  HO Wanki, ZHU Huaqun, YE Hua

  2025, 45(5): 627-632.

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  Peripheral helper T cells (Tph) have been identified in recent years as a CD4⁺T cell subset. Tph are characterized by the secretion of C-X-C motif chemokine ligand 13 (CXCL13), and the expression of surface molecules including PD-1, inducible costimulatory (ICOS), HLA-DR, etc. By expressing chemokine receptor C-C motif chemokine receptor 2 (CCR2), C-X3-C motif chemokine receptor 1 (CX3CR1), and CCR5, Tph can be recruited to inflammatory sites and promote the formation of tertiary lymphoid structures (TLS). Through interaction with IL-21 and signaling lymphocytic activation molecule family (SLAMF), Tph assist B cell maturation, differentiation, and antibody production. Tph are shown to be involved in the pathogenesis of many autoimmune diseases. Herein, this review discusses the biological characteristics of Tph and their role in different types of autoimmune diseases to further reveal their mechanism of action and clinical value, and provide new ideas for future targeted therapy.