30 January 2025, Volume 45 Issue 1

  

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  Current status and challenges of immunotherapy for multiple myeloma

  2025, 45(1): 1-6.

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  At present, multiple myeloma (MM) remains an incurable disease. In recent years, immunotherapeutic drugs, represented by CD38 monoclonal antibody, have been widely used in the clinical practice and significantly prolonged the survival of MM patients. Meanwhile, a variety of highly effective novel immunotherapeutic agents such as chimeric antigen receptor (CAR)-T cell, antibody-drug conjugate (ADC), and bispecific antibody (BsAb) are continuously emerging, reshaping the treatment landscape of MM. This review summarizes the current development and challenges in the field of immunotherapy for MM, while also offering reflections and suggestions on the future direction of immunotherapy, for providing the reference in the field of MM diagnosis and treatment research.
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  Host GPR84 promotes the formation of mycobacterial infection-induced lipid droplet and accelerates infection

  ZHOU Jing, Reziya·Wumaier, CHEN Zi-han, LIU Jian-xin, WANG De-cheng, YAN Bo

  2025, 45(1): 7-13.

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  To investigate the role of host G-protein-coupled receptor 84 (GPR84) upon mycobacterial infection, GPR84 mutant zebrafish model was established to assess the effect of GPR84 on Mycobacterium marinum (M.m.) proliferation and host survival. Mechanistically, the effect of GPR84 on macrophage and neutrophil development was first excluded by neutral red staining and Sudan black staining, respectively. The effect of GPR84 deficiency on neutrophil recruitment was evaluated by zebrafish tail amputation assay. Moreover, the formation of lipid droplets in infected zebrafish was detected by oil red O staining, and the transcription levels of genes related to lipid metabolism and inflammatory factors in infected models were detected by qRT-PCR. The results of the above experiments showed that transient knockout of GPR84 in zebrafish inhibited the proliferation of M.m. in vivo and prolonged host survival, whereas GPR84 deficiency did not affect the development of macrophages and neutrophils, or the recruitment of neutrophils. Further studies revealed that GPR84 mutant zebrafish presented reduced lipid droplets formation after mycobacterial infection and was accompanied by down-regulation of cholesterol efflux pump gene ATP-binding cassette transporter G1 (ABCG1), meanwhile inflammatory factors expression was up-regulated. This study suggests that mycobacterial infection may induce lipid droplets formation through host GPR84 to suppress inflammatory factors expression and ultimately facilitates the process of bacterial infection.
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  Identification and clinical significance of abnormally expressed serum cytokines in patients with systemic lupus erythematosus

  REN Ji-gang, ZHANG Xiao-min, LIU Chang, REN He-fei, ZHOU Lin

  2025, 45(1): 14-21.

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  This study aimed to screen and identify abnormally expressed cytokines in the serum of patients with SLE and to explore their clinical significance. Liquid-phase microarray technique was used to detect the expression differences of 45 cytokines spectrum in 3 SLE patients and 3 healthy individuals. Subsequently, ELISA was used to verify the most differentially expressed cytokines in 54 SLE patients and 28 healthy individuals, and their correlations with SLE disease activity index 2000 (SLEDAI-2K) score, typic laboratory indicators and renal involvement were studied. The results showed that a total of 15 cytokines were highly expressed in the sera of SLE patients, and 4 most significant differentially expressed cytokines were picked out  based on the fold differences. Further testing found that the serum levels of IL-6, IL-10, IL-1 receptor antagonist (IL-1Ra) and    IFN-γ-inducible protein 10 (IP-10) were significantly higher in SLE patients than in healthy controls(all with P＜0.05). Among them the serum levels of IL-10 and IL-1Ra were positively correlated with the SLEDAI-2K score in SLE patients. In addition, serum IL-10 levels were positively correlated with serum IgG and ESR, while the serum IL-1Ra levels were negatively correlated with complement C3 and complement C4(all with P＜0.05). Furthermore, the serum IL-1Ra levels were positively correlated with total  protein in urine within 24 hours (TPU)  in SLE patients(P＜0.001). Collectively, above data indicates that multiple cytokines were abnormally expressed in SLE patients. The serum levels of IL-10 and IL-1Ra are related to the disease activity of SLE, and the serum IL-1Ra  could be associated with SLE renal involvement. Detection of these indicators may provide proofs for clinical diagnosis, treatment, and monitoring of SLE.
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  Indolepropionic acid inhibits LPS-induced apoptosis and inflammation of peritoneal mesothelial cells by regulating NF-κB

  LI Hong-bo, TU Can, FU Shuai, JIANG Nan, DING Yan-qiong, XIONG Fei

  2025, 45(1): 22-26.

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  The aim of this study is to investigate the effect and mechanism of indolepropionic acid (IPA) on LPS-induced proliferation, apoptosis, and inflammatory response of peritoneal mesothelial cells. Firstly, mouse peritoneal mesothelial cells were treated with 0.1, 1.0, and 10 μmol/L IPA, respectively. After 24 h, CCK-8 method was used to detect the cytotoxicity of IPA. Next, cells were pretreated with 0.1, 1.0, and 10 μmol/L IPA for 2 h, followed by treatment of 10 mg/L LPS for 24 h. CCK-8 method was used to detect the proliferation ability of cells, and the optimal working concentration of IPA was determined. The cells were divided into 5 groups: control group, LPS group, LPS+IPA group, LPS+QNZ (a NF-κB pathway inhibitor) group, and LPS+QNZ+IPA group. CCK-8 method was used to detect cell proliferation, and flow cytometry was used to detect cell apoptosis. ELISA was used to detect the level of TNF-α in the cell supernatant, and Western blotting was used to detect the  expressions of NF-κB p65 and p-p65 in the cells. The results showed that 0.1 and 1.0 μmol/L IPA had no cytotoxicity on mouse peritoneal mesothelial cells, and the optimal working concentration of IPA was 1.0 μmol/L. Compared to those of control group, the proliferation ability of LPS group was significantly decreased (P<0.01), while the apoptosis rate, the level of TNF-α in the cell supernatant, and the phosphorylation level of NF-κB p65  in the cells were all significantly increased (P<0.01). Compared to that of the LPS group, the proliferation ability of LPS+IPA group, LPS+QNZ group, and LPS+QNZ+IPA group was significantly increased (P<0.01), while the apoptosis rate, the level of TNF-α in the cell supernatant, and the phosphorylation level of NF-κB p65  in the cells were significantly decreased (P<0.05). Therefore,LPS+QNZ+IPA combination showed the most significant effect. In summary, these results indicate that IPA promotes the proliferation of mouse peritoneal mesothelial cells induced by LPS, and inhibits cell apoptosis and inflammation. The underlying mechanism may be related to the inhibition of NF-κB pathway activation.
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  Curcumin reduces liver injury in rats with non-alcoholic fatty liver disease by regulating TNF-α/NF-κB signaling pathway through miR-155

  XIE Ping, LI Chan, LYU Kun

  2025, 45(1): 27-36.

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  The aim of this study is to investigate whether curcumin  reduces liver injury in rats with non-alcoholic fatty liver disease (NAFLD) by regulating TNF-α/NF-κB signaling pathway through miR-155. The effect of curcumin on the degree of injury of NAFLD rats was observed by histopathology. Changes in blood lipids and liver function were detected by serological tests, and levels of inflammatory factor (TNF-α) were detected by ELISA in rats in different groups.The expressions of TNF-α, inhibitor of NF-κB (IκBα), NF-κB p65 and p-NF-κB p65 were detected by qRT-PCR and Western blotting, respectively. The results showed that compared to those of the model group, the degree of steatosis and inflammation in livers of rats treated by different doses of curcumin or in the NF-κB inhibition group were all significantly reduced, and the tissue lesions degree was significantly alleviated. In addition, serum levels of alanine amino-transferase (ALT), triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were all significantly decreased (P<0.05), while total protein (TP), albumin (Alb), and high-density lipoprotein cholesterol (HDL-C) were all significantly increased (P<0.05). On the other hand, the release of TNF-α in both serum and liver tissues was significantly decreased (P<0.01), along with decreased relative expression of miR-155 and NF-κB p65 in liver tissues (P<0.01), and the relative expression of IκBα was significantly increased (P<0.01).In addition, the effect was more significant with combined intervention of curcumin and NF-κB inhibitor. This study suggests that curcumin may regulate TNF-α/NF-κB signaling pathway through miR-155 to reduce liver    injury in NAFLD rats.
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  Pachymic acid regulates inflammatory response in rats with chronic glomerulonephritis via the MCP-1/CCR2 signaling pathway

  XIE Yu-duan, LI Han-lian, HAN Yan, YU Ting, LI Wei

  2025, 45(1): 37-42.

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   The aim of this study is to investigate the impact of pachymic acid (PA) on inflammatory response in rats with chronic glomerulonephritis (CGN) by regulating monocyte chemoattractant protein 1(MCP-1)/CC chemokine receptor 2(CCR2) signaling pathway. Ten SD rats were randomly selected as the control group, and the rest were injected with cationic bovine serum albumin (C-BSA) to establish the CGN model. Successfully modeled rats were randomly divided into CGN group, PA group (10 mg/kg PA), GW0742 group (0.3 mg/kg GW0742), and PA+GW0742 group (10 mg/kg PA+0.3 mg/kg GW0742), with 10 rats in each group. 24-h urine protein, serum creatinine(Scr), blood urea nitrogen (BUN), antioxidant index and inflammatory index were detected with the corresponding commercial kits. The pathological injury of renal tissue was  detected by H-E staining, and the levels of IgG and C3 in glomerulus were detected by immunofluorescence staining. The mRNA expressions of MCP-1 and CCR2 were detected by qRT-PCR. Western blotting was used to detect the expressions of MCP-1/CCR2 signaling pathway related proteins. The results showed that rats in the control group had normal renal tissue whereas in the CGN group, both capillary rings and Bowman sacs were thickened, and degeneration of renal tubular epithelial cells and infiltration of inflammatory cells were observed. Compared to those of the control group, the levels of 24-h urine protein, Scr, and BUN, the levels of IL-1β and TNF-α, degree of renal tissue injury, fluorescence relative intensity of IgG and C3, and the mRNA and the protein levels of  MCP-1 and CCR2  in the CGN group significantly increased(P<0.05), while the levels of superoxide dismutase (SOD)and glutathione (GSH) significantly decreased (P<0.05). PA was shown to improve the above indicators, while GW0742 induced opposite changes of these indicators compared to those of the PA group. GW0742 attenuated the improvement effect of PA on inflammatory response in CGN rats. This study suggests that PA may improve the inflammatory response of CGN rats by down-regulating MCP-1/CCR2 signaling pathway.
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  Establishment and performance evaluation of Aspergillus IgG antibody detection based on chemiluminescence immunoassay

  SUN Ya-shun, ZHAO Si-qi, LI Jing-jing, LIU Chun-long, MA Long

  2025, 45(1): 43-46.

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   In order to explore the efficacy of chemiluminescence immunoassay for the detection of Aspergillus IgG antibody, a method was established to enable the rapid detection of Aspergillus IgG antibody based on the indirect chemiluminescence principle with streptavidin magnetic particles as carrier, biotinylated Aspergillus galactomannan (GM) antigen as capture antigen, and alkaline phosphatase-labeled sheep anti-human IgG antibody as detection antibody. In addition, the assay performances of the method such as cut-off value, blank limit, detection limit, precision, interference test, cross-reactivity, methodological comparison, etc. were evaluated. The results showed that the detection efficacy of Aspergillus IgG antibody was performed favorably with a cut-off value of 120 AU/mL, a blank limit of 5.0 AU/mL and a detection limit of 5.2 AU/mL. The coefficients of variation of the reagent precision were <10%. The relative deviations of the test results for high concentrations of hemoglobin, bilirubin and triglyceride in the samples were less than 10%, and no cross-reactivity was observed. The data generated by this method was consistent with that of the ELISA kit (r=0.982, Kappa=0.87, P=0.00). Altogether, this study established a novel chemiluminescence-based immunoassay for the detection of Aspergillus IgG antibody, and the performance parameters of the assay system meet the clinical requirements and are suitable for the rapid detection of Aspergillus IgG antibody in serum.
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  A magnetic particle chemiluminescence immunoassay for the detection of Candida mannan

  FENG Su-ya, MA Long, ZHANG Zhou, ZHANG Yi-fan

  2025, 45(1): 49-54.

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  A magnetic particle chemiluminescence immunoassay (MPCLIA) for the detection of Candida mannan (Mn) was established. Monoclonal antibody was prepared by immunizing BALB/c mice with Candida Mn as antigen. The MPCLIA for Candida Mn detection was established by using automatic chemiluminescence analyzer and double-antibody sandwich method. The complex of streptavidin-magnetic particle-biotin labeled-Candida Mn-acridine sulfonamide labeled antibody was formed in the reaction system. The results showed that the limit of blank (LoB) was 2.0 pg/mL and the limit of detection (LoD) was 5.0 pg/mL. The linear range was 10.0~1 000.0 pg/mL. The variation coefficients of repeatability and of precision  were both less than 10%. The recovery rate was 85%～115%. When the concentrations of hemoglobin, bilirubin or triacylglycerol (TAG) reached 7 mg/mL, 300 mg/L and 7.5 mmol/L, respectively, there was no significant interference on the laboratory results. The results generated with this method were in line with clinical diagnosis outcomes (κ=0.79). Altogether, the Candida Mn MPCLIA established in this study has met the detection standards for in vitro diagnostic reagents, and  is expected to become a rapid immunological detection method of Candidiasis after  sufficient sample data promise.
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  Analysis of clinical distribution of the lupus anticoagulant detection

  YAN Nan, LIU Jia-yun, DIAO Yan-jun

  2025, 45(1): 55-59.

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  The clinical data of 1 431 patients with lupus anticoagulant (LA) from Air Force Military Medical University Affiliated Xijing Hospital were collected to analyze the distribution  characteristics of LA in 4 major clinical departments and in disease types. Lab reports of the 1 431 cases with LA were retrospectively analyzed and patients were divided into 4 groups according to the affiliated clinical departments: A, B, C, and D. The percentage of detected size, LA positive rate, LA ratio median (M) and percentile (P) (P25, P75), 95% confidence interval (CI), and the percentage of disease types with positive results in groups A, B, C, and D were compared.The results showed that, among the 1 431 patients with LA report in the hospital, department of immunology （group A） accounted for the highest proportion (53%), with LA positive rate of 41%, M and 95% CI of 1.17 and 1.01～1.95, respectively, and the disease type was mainly SLE (33%). The obstetrics and gynecology reproductive center（group B） ranked second (35%) in patient number, and the positive rate was 29%, with M and (P25, P75)［1.15(1.10, 1.21)］ and 95% CI (1.01～1.42) being the lowest. Among the 4 groups, group C (department of emergency) had the highest positive rate (43%), and the M and (P25, P75)were the greatest ［1.19(1.10,1.36)］, with SLE encephalopathy (SLEE) being the dominant disease type for this group (37%). The 95% CI for group D was 1.01 to 2.98, owning the largest variation. In conclusion, among the 1 431 patients with  LA outcomes in Xijing hospital, SLE was the main disease type, among which SLEE from the department of neurology and lupus nephritis (LN) found in the department of nephrology were the most common and serious complications of SLE. In brief, prior to the detection of LA, it is necessary to fully evaluate whether patients meet the indications for detection, and further relevant examinations should be carried out in positive patients to avoid falling and misdiagnosis.
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  Study on the mechanism of targeting miR-221 to regulate STAT3-mediated immune escape in lung cancer cells

  CHEN Xuan, SHAO Yi, ZOU Jia-hua

  2025, 45(1): 60-64.

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  This study aims to explore the regulatory effect of endogenous miR-221 on STAT3 and the molecular mechanism of immune escape in lung cancer cells. Quantitative PCR was used to detect the expressions of miR-221 and STAT3 mRNA in lung cancer tissues and adjacent normal tissues, and the correlation between miR-221 and STAT3 mRNA expression in cancer tissues was analyzed. Luciferase reporter system was used to determine the regulatory effect of miR-221 on STAT3. A549 lung cancer cells were cultured in vitro and divided into control group (mimic control group), miR-221 high expression group (miR-221 mimic transfection), and miR-221 low expression group (anti-miR-221 transfection). The expressions of STAT3 and p-STAT3 protein in each group were compared. The transfected cells were co-cultured with NK-92 cells at a ratio of 1∶5 and the expressions of IL-2, IFN-γ, and TNF-ɑ in culture supernatant were compared. The immune killing rate of NK-92 cells was also measured. The results showed that the expression levels of miR-221 and STAT3 mRNA in lung cancer tissue were significantly higher than those of the adjacent tissue, and there was a positive correlation between miR-221 and STAT3 mRNA in lung cancer tissue (P<0.05). Luciferase assay showed that miR-221 targeted and upregulated the expression of STAT3. The protein expressions of STAT3 and p-STAT3 in the miR-221 low expression group were lower than those of the control group and the high expression group. The protein levels of STAT3 and p-STAT in the high expression group were even higher than those of the control group (P<0.05). The immune killing rate of NK-92 cells and the secretion of IL-2, TNF-α and IFN-γ in the miR-221 low expression group were higher than those of the control group and the high expression group while these indicators in the miR-221 high expression group was lower than those of the control group (P<0.05). In conclusion, miR-221 is highly expressed in non-small cell lung cancer tissue, and upregulation of its expression can inhibit the killing activity of NK cells. The underlying mechanism may be related to the STAT3 mediated immune escape of lung cancer cells.
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  The biological function of PD-L2 and research progress on related diseases

  SONG Sai-zhe, DING Si-si, LIU Cui-ping

  2025, 45(1): 65-69.

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  PD-L2 binds to PD-1 to inhibit T cell proliferation and cytokine production, while its interaction with repulsive guidance molecule b (RGMb) has the opposite effect. Researches revealed that PD-L2 is abnormally expressed in the peripheral blood and corresponding tissues of patients with tumors or autoimmune diseases, and participates in disease progression by glycosylation modifications and interactions with immune cells. In order to fully understand the regulation and expression of PD-L2 and its regulation on tumors and autoimmune diseases after binding to receptors, this review first elucidates the biological characteristics of PD-L2 and discusses its involvement in disease progression, then summarizes the research progress of PD-L2 on cancer and autoimmune diseases, and finally summarizes the prospect of its research value, aiming to provide new ideas for the research and treatment of various diseases including tumor.
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  Research progress on the role of lipocalin 2 in Alzheimer's disease

  WANG Meng-fei, YUAN Yong, JIA Ya-quan, ZHANG Zhen-qiang, SONG Jun-ying

  2025, 45(1): 70-73.

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  Alzheimer's disease (AD) is a slowly progressing and hard to diagnose degenerative disease of the central nervous system. Its pathological characteristics and pathogenesis are very complex, mainly involving amyloid-β peptide (Aβ) deposition,Tau protein hyperphosphorylation, neuroinflammation and many other aspects. In recent years, it has been found that lipocalin-2  (Lcn2), an inflammatory protein involved in immune regulation and iron ion transportation, directly or indirectly promotes brain neuroinflammation, iron accumulation and blood-brain barrier function damage in the development of AD. From the above aspects, this review summarizes the relationship between Lcn2 and AD.
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  Research progress on genetic susceptibility genes related to celiac disease

  XUE Sheng-long, SHI Tian, GAO Feng

  2025, 45(1): 74-81.

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  Celiac disease (CeD) is a type of intestine autoimmune disease caused by the intake of grains containing gluten protein in susceptible gene carriers. Genetic factors play an important role in the pathogenesis. Almost all CeD patients carry HLA-DQ2/DQ8, which accounts for about 40% of the disease genetic causes, while the remaining 60% of cases are attributed to a large number of non-HLA genes. The genome-wide association study (GWAS) has found that over 50 non-HLA genes are associated with CeD pathogenesis, but currently discovered non-HLA genes can only explain about 15% of genetic susceptibility, and there are a large number of non-HLA genes that yet to be discovered. This review focuses on the research progress of CeD susceptible genes, providing ideas and methods for a deeper understanding of the pathogenesis of CeD and for subsequent diagnosis and therapy.
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  Research progress on the regulation of HBx on lncRNA in the development of HCC

  TIAN Xu-yun, LIU Lin, ZENG Yi, LUO Hao-xiang

  2025, 45(1): 82-88.

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  Hepatocellular carcinoma (HCC) is one of the most common malignancies, and the main risk factor for HCC is HBV infection. Hepatitis B virus X protein (HBx) is a key regulator of HBV-associated HCC and can promote tumorigenesis. It has been reported that many long non-coding RNA (lncRNA) contribute to the HCC development, mainly by promoting HBV replication, up-regulating oncogenes expression, or down-regulating the expression of tumor suppressors.Some lncRNA can also act directly as tumor suppressors, which have been extensively studied as disease-treating targets.In this review, we will discuss the role of HBx-regulated lncRNA in HBV-induced HCC and summarize the mechanisms of tumorigenesis and the development of cancer.