[Immune tolerance inducing effects of soluble human leucocyte antigen G1 on natural killer cells and T cells].

OBJECTIVE: To investigate the immune tolerance inducing effects of soluble human leucocyte antigen G1 (sHLA-G1) on natural killer (NK) cells and T cells. METHODS: A recombinant plasmid expressing sHLA-G1 was constructed and transfected into human lymphoblastoid cells LCL721.221. sHLA-G1 in the supernatant was purified by immuno-affinity chromatography and then added into the culture of NK cells obtained from the peripheral blood mononuclear cells of 3 unrelated individuals. Target cells, K562 cells, were added too. The killing rate of NK was calculated. Peripheral blood lymphocytes (PBLs) were obtained and stimulated by Ebstein-Barr-virus-transformed B lymphoblastoid cell line (EBV-LCL). The proliferation of the T cells in the mixed lymphocyte culture was examined by enzyme linked immunosorbent assay. The antigen-specific T cells in the peripheral blood was activated. sHLA-G1 was added into the culture. Then the T cells were suspended in the solution of fluorescence isothiocyanate (FITC)-annexin-V. Flow cytometry was used to detect the fluorescent intensity of FITC so as to examine the apoptosis of T cells. RESULTS: sHLAG-1 inhibited the cytotoxicity of NK cells dose-dependently. sHLAG-1 inhibited the proliferation of activated T cells, and induced the apoptosis of T cells dose-dependently, with a dose-saturation character and without antigen-specificity. CONCLUSION: sHLAG-1 is a kind of immune tolerance inducing molecule.

Expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patient.

AIM: To investigate the expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patients. METHODS: The expression of local renin and angiotensinogen mRNA in the liver, splenic artery and vein of PH patients was detected by RT-PCR analysis. RESULTS: Expression of local renin mRNA in the liver of control group was (0.19+/-0.11), significantly lower than that in splenic artery (0.45+/-0.17) or splenic vein(0.39+/-0.12) respectively, (P<0.05). Expression of local angiotensinogen mRNA in the liver was (0.64+/-0.21), significantly higher than that in splenic artery(0.41+/-0.15) or in splenic vein (0.35+/-0.18) respectively, (P<0.05). Expression of local renin mRNA in the liver, splenic artery and vein of PH group was (0.78+/-0.28), (0.86+/-0.35) and (0.81+/-0.22) respectively, significantly higher than that in the control group, (P<0.05). Expression of local angiotensinogen mRNA in the liver, splenic artery and vein of PH group was (0.96+/-0.25), (0.83+/-0.18) and (0.79+/-0.23) respectively, significantly higher than that in the control group, (P<0.05). There was no significant difference between the liver, splenic artery and vein in the expression of local renin or local angiotensinogen mRNA in PH group, (P<0.05). CONCLUSION: In normal subjects the expression of local renin and angiotensinogen mRNA was organ specific, but with increase of the expression of LRAS, the organ-specificity became lost in cirrhotic patients. LRAS may contribute to increased resistance of portal vein with liver and formation of splanchnic vasculopathy.