| objective: Basal and clinical studies have showed that, costiniulatory molecules CD86 and CD8O, which belong to the B7 family, maybe take important roles in the initiation and progress of systemic lupus erythematosus(SLE), blockade this signaling pathway can prevent the occurrence of mouse lupus or relieve the illness state. The functions of B cells to present auto-antigens and activate Th cells are possibly one of the key points. To investigate the abnormalities in the costimulatory signaling pathway of SLE B cells, percentage of CD86~ and CD8O~ B cells in peripheral blood mononuclear cells(PBMC) of SLE patients were measured and compared with those of normal controls in the present study. In addition, PBMC of SLE patients and normal controls were cultured in vitro with or without the presence of triptolide(TL), one of the main effective components of tripterygium glycosides, in order to study its effects on the expression of B7 molecules on B cells. Methods: Eleven SLE patients in remission and eleven age- and gender-matched normal controls were studied. Lymphocyte separating medium was used to separate PBMC, flow cytometer and fluorescence labelled mouse-anti-human monoclonal antibodies(combination of anti-CD19-FITC and anti-CD86-PE or anti-CD 1 9-FITC and anti-CD8O-PE) were usd to measure the rate of CD86 or CD80 B cells. PBMC was cultured in culture medium consisting RPMI164O supplemented with 10% calf serum, L-glutamine, antibiotics, and TL of different concentration. Flow cytometer analysis was carried out after 48 hours. The same culture method was used to study TL抯 effects on proliferation of PBMC. Results: (1) In the freshly separated PBMC from SLE patients, the percentage of CD86 B cells was found to be much higher than that of normal controls(P<0.00 1), whereas the average percentage of CD80 B cells in SLE patients was also higher but not statistically significant. (2) IL significantly suppressed the proliferation of PBMC from SLE patients or normal controls. The incorporation of 3H-TdR showed a reduction of 82.82 l0.89(%)/82.18 .72(%) in SLE/normal people. (3) 2.5ngIml IL could down-regulate the percentage of SLE CD86 B cells(P<0.00 1), but not that of CD80 B cells or normal controls CD86 and CD8O B cells.(4) 25ng/ml IL could down-regulate CD86 or CD80 percentage of SLE or normal B cells. Interestingly, IL's effect on SLE CD8O , but not CD86 (although average reduction percentage higher), B cells was statistically more than on normal controls JP<0.05). Conclusion: (1) CD86 B cells of SLE patients PBMC are more than that of normal people, and inspite of not being statistically significant, data show the same tendency in SLE patients. This phenomenon may reflect the importance of CD281B7 signaling pathway in the initiation and/or progress of human SLE. (2) IL can effectively suppress the proliferation of lymphocytes. There is no difference between its effect on SLE patients and on normal people. (3) The experimental results implicated that IL has a significant effect on reducing B7 costimulatory signals from B cells, and may consequently reduce the degree of autoimmunity in SLE. (4) 2.5ng/ml may be the minimal concentration of IL to be effective. (5) IL was more effective on reducing SLE CDSO+ B cells compared with normal people, so it's implied that II. suppresses normal immune response to a less degree.
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