Objective To investigate the effect of iuvenile rheumatoid arthritis(JRA) serum (leukotriene B4,LTB4) LTB4-BLT2 on mice DCs.Methods Bone marrow(BM)-derived DCs from healthy mouse were purified.and induced by cytokine IL-4 and GM-CSF to immature DCs and then differentiated to mature DCs under the stimulation of LPS in vitro.DCs were evaluated by light microscope and flow cvtometry.The concentrations of LTB4 in DCs supernatant,normal serum,active JRA,and that of the co-cuItured with BLT2 antagonist LY255283 were detected by ELISA.The expression of BLT2 protein and mRNA in DCs was examined by immunocytochemistry,immunofluorescence and RT-PCR.Meanwhile,the expression of BLT2 in DCs after 18 h co-cultured with normal serum,in serum of active JRA and that of BLT2 antagonist (LY255283)group was assayed by flow cytometry respectively.Results LTB4-BLT2 was expressed by DCs.Not only BLT2 mRNA but also its protein was expressed in DCs.The concentration of LTB4 Was(17±3)pg/ml,(82±20)pg/ml,(82±20)pg/ml and(24±6)pg/ml,(115±20)pg/ml,(91±11)pg/ml in normal serum group,active JRA group and LY255283 group before and after 1 8 h,respectively.The expression Was higher in serum of active JRA group than that of normal sertlm group(P<0.01)and there was a tendency to be higher when compared with LY255283 group(P<0.05).The DC BLT2 expression was 27.7±2.9,46.3±8.7 and 30.3±5.5 in normal serum group,serum of active JRA group and LY255283 grbup after 1 8h respectively.The expression was stronger in active JRA group than other groups(P<0.05).Conclusion DC can develop a LTB4-BLT2 signal pathway by BLT2 with autocrine and/or extrinsic LTB4.The overexpression of this pathway may be involved in the initiating and activation of JRA.

Objective:To explore the role of TNFSF14 and its receptors LTβR and HVEM in the pathogenesis of virus hepatitis.Methods:Marine fulminant viral hepatitis model was established by infecting mice with MHV-3.Liver tissue destruction in LIGHT KO and WT mice were analyzed by HE staining and ALT levels in serum by automatic biochemical analyzer .The mRNA levels of HVEM and LTβR in the liver and spleen tissues in the indicated time points ( 0 h, 12 h, 24 h, 48 h, 72 h ) were detected by quantitative-PCR.The expression of HVEM and LTβR on PBMC in patients with severe hepatitis were measured by flow cytometry.Results:In the MHV-3-induced murine fulminant hepatitis model ,liver injury in LIGHT KO mice was obviously decreased than that of WT mice,and ALT levels was also significantly lower than that of WT mice (P<0.01).The mRNA of HVEM and LTβR in the spleen were increased significantly after 48 h postinfection with MHV-3 ( P<0.05 );The level of LTβR mRNA in liver was significantly up-regulated in 12 h postinfection with MHV-3(P<0.01).Compared to healthy volunteers,the expression of both HVEM and LTβR on PBMC in patients with severe hepatitis was remarkably enhanced .Conclusion: TNFSF14 and its receptors LTβR and HVEM play a critical role in the pathogenesis of viral fulminant hepatitis .