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Objective: To observe the effect of recombination human TACI-Ig (rhTACI-Ig) on the activation of mice T lymphocytes induced by anti-CD3, and to clarify the potential mechanism at the same time.Methodes: Putified T lymphocytes from the spleens of C57BL/6 mice by immunomagnetic beads were treated with anti-CD3 antibody with or without different concentrations of rhTACI-Ig, recombinant human tumor necrosis factor-α receptor Ⅱ ∶IgG Fc(rhTNFR:Fc) or IgGFc.The proliferation of T lymphocytes was determined by [3H]-TdR incorporation, the levels of interleukin-2(IL-2)、 IL-4、 interferon-γ(IFN-γ)、 transforming growth factor-β (TGF-β) in cell supernatant were detected by ELISA, the percentages of CD4/CD154+, CD4+/CD69 and CD4+/CD62L+ T lymphocytes were tested by flow cytometry.Western blot was applied to evaluate the expression of B cell activating factor receptor(BAFFR) and TACI.Results: As expected, anti-CD3 obviously induced the activation of T lymphocytes by promoting proliferation, IL-2, IFN-γ, IL-4 and TGF-β secretion, and increasing CD4+/CD154+, CD4+/CD69 T lymphocytes population, but decreasing the percentage of CD4+/CD62L+ T lymphocytes.Anti-CD3 induced T lymphocytes over activation were significantly inhibited by either rhTACI-Ig or rhTNFR:Fc treatment, but not IgGFc.rhTACI-Ig decreased the upregulated expression of BAFFR and TACI in anti-CD3 stimulated T lymphocytes.Conclusion: RhTACI-Ig blocked the extensive activation of T lymphocytes, which were stimulated in an antigen-presenting manner in vitro, through regulating the signaling of BAFFR and TACI.