Expression Of CXCL16and CXCL10Correlates With Disease Activity In Lupus Nephritis Patients

Background and ObjectiveSystemic lupus erythematosus (SLE) is a systemic autoimmune disease with thepotential to affect a variety of organs and correlates with circulating immune complex.Lupus nephritis (LN) is one of the most frequent manifestations of SLE and can bepresent in100%of SLE patients The disease is linked to the expressions of manycytokines including chemokines. Chemokines mediate the balance of cytokines anddevelopment of disease. CXC chemokine ligand16(CXCL16) was expressed onmacrophage, dendritic cell (DCs), mononuclear leucocytes and B cells and can bind toits only receptor CXC receptor6(CXCR6).CXCL16and CXCR6function in antigenpresenting cells (APC)-T cells interactions and initiate immunoreactions. Similarly, themigrations of activated T cells and NK cells into the inflammatory tissues are dependenton CXC chemokine ligand10(CXCL10) and its receptor CXC receptor3(CXCR3). Inthis study, we examined the concentrations of CXCL16and CXCL10in urine, serumand localized the intrarenal expressions of CXCL16in LN patients in order to found aconvenient means of detection for the clinical judgment of LN activity.MethodsThe serum and urine samples of76SLE hospitalized patients in NephrologyDepartment of Hospital from March,2012to March,2013were recruited in the study.14health people were signed as normal controls. The serum and urine levels ofCXCL10, CXCL16were assessed by enzyme-linked immuno sorbent assay (ELISA)in LN patients and normal controls. Among76SLE patients,41patients were diagnosed lupus nephritis by kidney biopsy, including7III LN,26IV LN and8V LN.Controls were taken from healthy parts of renal tissue from10tumor nephrectomies.Immunohistochemistry was used to detect the renal tissue expressions of CXCL16inpatients and healthy controls.Results1.The serum concentrations of CXCL10and CXCL16were significantly higher inLN patients than those in healthy controls(P﹤0.01).In addition, the levels of serumCXCL10showed positive correlation with SLEDAI and negative correlation withserum C3level (P﹤0.01) and no correlation with AI, CI, the count of white blood cells,thrombocytes, immunoglobulin, C4,24urine protein quantitation. The levels of serumCXCL16showed no correlation with acute index(AI), chronic index(CI), SLE diseaseactivity index(SLEDAI), the count of white blood cells and thrombocytes,immunoglobulin, C4,24hour protein quantitation.2. The urinary levels of CXCL10and CXCL16were significantly higher in LN patientsthan those in healthy controls(P﹤0.01).The levels of urine CXCL16showed positivecorrelation with SLEDAI (P﹤0.01) and correlated positively with the AI in Ⅳ LN.Theurinary levels of CXCL10showed no correlation with all clinical index.3. In healthy renal tissues CXCL16were distributed mainly in renal tubules and rarelyseen in glomerular cells while the expressions in renal tubules increased and glomerulistainings were found in LN paitients.CXCL16expressed significantly in LN patientsthan normal controls(P﹤0.05).Besides, different concentrations of CXCL16wereobserved in Ⅲ,Ⅳ and Ⅴ LN, the expressions of CXCL16in Ⅳ LN were higherthan those in Ⅲ LN and Ⅴ LN(P﹤0.01),while no difference between the Ⅲ LNand Ⅴ LN. ConclusionThe serum and urine, expressions of CXCL16and CXCL10in SLE patients areincreased markedly. The urinary levels of CXCL16showed positive correlation withSLEDAI and renal AI positively and the change of CXCL16concentrations in kidneywas associated with the pathology category of LN. The levels of CXCL16in urine maybe useful as marker of disease activity.