| Objective: Lupus nephritis(LN)is the most common and serious complication of systemic lupus erythematosus(SLE).Its clinical manifestations are complicated and diverse,including proteinuria,hematuria and cylindruria,accompanied by hypertension,edema,etc.,and the disease can be gradually extended to end-stage renal disease(ESRD).The pathogenesis of LN is complex,and the exact mechanism remains unclear.However,many cytokines promote the production of autoantibodies,the formation of immune complexes and the infiltration of inflammatory cells in the kidney,leading to the development and progression of renal disease.Therefore,the changes of cytokine network play an important role in the pathogenesis of LN.Th17 cells are a group of newly discovered CD4 + T cells,which play an important role in a variety of autoimmune diseases.In recent years,the study found that Th17 cells also play a role in the pathogenesis of LN that can not be ignored.Interleukin-17(IL-17)is a major cytokine secreted by Th17 cells and has a strong proinflammatory effect.IL-17 can not only promote the production of various growth factors and chemokines,but also has a synergistic effect with cytokines such as interleukine-6(IL-6)to expand the local inflammatory response,and it has the ability to recruit neutrophils to the local inflammatory site,so as to further strengthen the tissue immune injury.Interleukin-23(IL-23)is a proinflammatory cytokine secreted by dendritic cells,which induces Th17 cell proliferation and differentiation and maintains its function in vivo.Studies have shown that IL-23 / IL-17 inflammatory pathways play an important role in a variety of autoimmune diseases.Tumor necrosis factor-like ligand 1A(TL1A),a member of the tumor necrosis factor superfamily,is a T cell costimulatory factor derived from endothelial cells.Studies have shown that TL1 A can act on Th17 cells and promote its ability to secrete IL-17,thereby enhancing the immune and inflammatory response.The aim of this study was to investigate the changes of IL-17,IL-23 and TL1 A in serum of patients with LN,and to analyze the relationship between IL-17,IL-23 and TL1 A and the relationship between them and clinical related indicators and LN activity to further explore the important role in the pathogenesis of LN.Methods: In this study,90 subjects,LN group,chronic nephritis group and healthy control group were selected.The research project was aprroved by the ethics committee of the hospital.The serum levels of IL-17,IL-23 and TL1 A in the three groups were detected by ELISA.Analyse and compare the relationship between the LN patient's research indicators and the relevant laboratory indicators and the correlation between the three groups.The data are analyzed by t test,Chi-square test and Spearman correlation analysis by using SPSS.19.0,P<0.05 represents statistical significance.Results:1.The level of serum IL-17 in LN group was obviously higher than that in chronic glomerulonephritis and healthy control [(40.701±26.851)ng/L vs(21.947±7.341)ng/L,P<0.05;(40.701±26.851)ng/L vs(14.788±4.839)ng/L,P<0.05)].The level of serum IL-17 in chronic glomerulonephritis was obviously higher than that in healthy control [(21.947±7.341)ng/L vs(14.788±4.839)ng/L,P<0.05)].The level of serum IL-17 in LN active group was also obviously higher than that in non-active group [(49.754±30.018)ng/L vs(27.122±13.149)ng/L,P<0.05].The levels of serum IL-17 in LN group showed negative correlation with the 1evel of serum albumin and C3(P<0.05),and showed positive correlation with urine macroalbumin(MA),24 hours protein quantification and anti ds-DNA antibody.But the levels of serum IL-17 in LN group showed no significant correlation with the 1evel of hemoglobin,platelets and SLEDAI(P>0.05).Indicating that elevated serum IL-17 may be involved in the inflammatory response and immune injury process of LN,and associated with LN activity.2.The level of serum IL-23 in LN group was obviously higher than that in chronic glomerulonephritis and healthy control [(292.076±143.052)ng/L vs(210.803±72.477)ng/L,P<0.05;(292.076±143.052)ng/L vs(157.084±38.697)ng/L,P<0.05)].The level of serum IL-23 in chronic glomerulonephritis was obviously higher than that in healthy control [(210.803±72.477)ng/L vs(157.084±38.697)ng/L,P<0.05)].The level of serum IL-23 in LN active group was also obviously higher than that in non-active group [(361.836±145.421)ng/L vs(187.437±36.875)ng/L,P<0.05].The levels of serum IL-23 in LN group showed negative correlation with the 1evel of hemoglobin,platelets,serum albumin and C3(P<0.05),and showed positive correlation with urine macroalbumin(MA),24 hours protein quantification,anti ds-DNA antibody and SLEDAI.The level of serum IL-23 in proliferative LN patients was increased compared with non-proliferative LN patients,and the difference was statistically significant(P<0.05).The level of IL-23 in serum of patients with LN was significantly correlated with the level of IL-17(P <0.01).Indicating that elevated serum IL-23 may reflect the activity of LN patients and the IL-23 / IL-17 inflammatory pathways may play an important role in the pathogenesis of LN.3.The level of serum TL1 A in LN group was obviously higher than that in chronic glomerulonephritis and healthy control [(4.072±2.273)ng/ml vs(2.734±1.350)ng/ml,P<0.05;(4.072±2.273)ng/ml vs(2.344±0.752)ng/ml,P<0.05)].The level of serum TL1 A in chronic glomerulonephritis showed no significant difference than that in healthy control [(2.734±1.350)ng/ml vs(2.344±0.752)ng/ml,P>0.05)].The level of serum TL1 A in LN active group was also obviously higher than that in non-active group [(5.204±2.271)ng/ml vs(2.373±0.639),P<0.05].The levels of serum TL1 A in LN group showed negative correlation with the 1evel of hemoglobin,platelets,serum albumin and C3(P<0.05),and showed positive correlation with urine macroalbumin(MA),24 hours protein quantification,anti ds-DNA antibody and SLEDAI.The level of IL-23 in serum of patients with LN was significantly correlated with the level of IL-17(P <0.01).Serum TL1 A levels were significantly correlated with serum levels of IL-17 and IL-23(P <0.01).Indicating that elevated serum TL1 A levels may synergistically enhance IL-23 / IL-17 inflammatory axis and be involved in the inflammatory response and immune injury process of LN.Conclusions:1.IL-17 is involved in the pathogenesis of LN through inflammatory pathways and can be used as a reference index of LN activity.2.IL-23 / IL-17 inflammatory axis promotes glomerular disease,and further confirms that the inflammatory axis plays an important role in the pathogenesis of LN;3.TL1 A promotes the inflammatory response and immunohistochemical damage process during the course of LN infection by synergistically promoting IL-23 / IL-17 inflammation. |
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