The Role Of Lectin Pathway In The Pathogenesis And Development Of Lupus Nephritis

BackgroundLupus nephritis（LN）,a complication of systemic lupus erythematosus（SLE）,is an immune complex nephritis.It is characterized by the production of a large number of autoantibodies and the deposition of immune complexes in renal tissues.It has been found that overactivation of complement system or regulatory imbalance are involved in the pathogenesis and progression of LN.As one of the important pathways of complement system,lectin pathway（LP）has no definite relationship with the pathogenesis and progression of LN.ObjectiveAnalyze the expression of LP complement factors in renal tissue of LN.To explore the role of LP in the pathogenesis and progression of LN.MethodsClinical data collection: renal biopsy was performed in the first affiliated Hospital of Xinxiang Medical University from May 2017 to March 2022.A total of 113 patients with LN were diagnosed clinically and pathologically.The clinical data and renal pathological reports of 113 patients were collected.The patients with LN were classified according to renal pathological types.Type I and II were defined as the mild LN,while type III,IV,V,III+IV and V+IV were defined as the severe LN.The renal pathological report included the pathological type of LN and the results of immunofluorescence.Immunohistochemical experiment: 30 cases of LN diagnosed by renal puncture were taken as LN group,20 cases of Immunoglobulin A nephropathy（Ig AN）diagnosed by renal puncture and 10 cases of inpatient urological surgery for nephrectomy of renal tumors（paracancerous normal renal tissues）were taken as control.30 cases of LN in the experimental group were regrouped according to the specific renal pathological type: 10 cases in the mild LN group and 20 cases in the serve LN group.The expression levels of LP complement factors Mannose-binding lectin（MBL）,Collectin-11（CL-11）,Ficolin-3 and Mannan-binding lectin-associated serine protease-2（MASP-2）in renal tissues were detected by immunohistochemistry.Results1 Renal pathological type: There were 113 patients with LN were definitely diagnosed,including 2 cases of type I,9 cases of type II,7 cases of type III,77 cases of type IV,6cases of type V,4 cases of type III + IV and 8 cases of type V + IV.The most pathological type of LN was type IV（68.14%）.2 Clinical data: Grouping 113 cases of LN according to renal pathological type,10 cases were female in 11 cases of the mild LN（90.91%）,80 cases were female in 102 cases of the severe LN（78.43%）.Compared with the mild LN,the serum creatinine and serum urea were significantly increased in the severe LN（P<0.01）.The percentage of LN with reduced serum C3 and C4 levels was 89.38% and 71.68% in 113 cases.The severe LN showed a downward trend compared with the mild LN.3 Immunofluorescence: The immunofluorescence negative expression of C1 q in renal tissue was 7.97%（9 cases）in 113 cases of LN,27.27%（3 cases）in the mild LN and 5.88 %（6 cases）in the severe LN.There was no significant difference in the expression level of complement factor C1 q in renal tissue between mild and severe LN（P>0.05）.4 Immunohistochemical analysis: The total renal integral optical density（IOD）of LP complement factors MBL,CL-11 and MASP-2 in LN was higher than that in paracancerous normal renal tissues and lower than that in Ig AN（P<0.05）.There was no significant difference in total renal IOD of Ficolin-3 between groups（P>0.05）.The total renal IOD of LP pathway complement factors CL-11,Ficolin-3 and MASP-2 in the severe LN were higher than those in the mild LN（P<0.05）.There was no significant difference in total renal IOD of MBL between groups（P>0.05）.MBL,CL-11,Ficolin-3 and MASP-2 were mainly expressed in renal tubules.ConclusionsMBL,CL-11 can bind to MASP-2 and activate LP,which is related to the pathogenesis of LN.CL-11,Ficolin-3 can bind to MASP-2 and activate LP,which is related to the development of LN.