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首页> 外文期刊>Ocular immunology and inflammation >Splenic T cells from mice receiving intracameral antigen suppress in-vitro antigen-induced proliferation and interferon-gamma production by sensitized lymph node cells.
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Splenic T cells from mice receiving intracameral antigen suppress in-vitro antigen-induced proliferation and interferon-gamma production by sensitized lymph node cells.

机译:来自接受前房内抗原的小鼠的脾T细胞抑制致敏的淋巴结细胞体外抗原诱导的增殖和干扰素-γ的产生。

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摘要

PURPOSE: To characterize the immunoregulatory mechanisms in vitro of spleen cells that are activated by intracameral injection of antigen (AC-spleen cells). Methods: AC-spleen cell regulation of in-vitro antigen-induced proliferation and interferon-gamma production by lymph node cells from TNP-BSA-immunized mice was quantified by co-culture of the lymph node cells with TNP-BSA and AC-spleen cells induced by intracameral TNP-BSA. Cytokine production was quantified by ELISA. RESULTS: AC-spleen cells produced significantly more IL-4 and IL-10 than spleen cells from TNP-BSA-immunized mice or naive spleen cells; unlike spleen cells from immunized mice, AC-spleen cells did not produce IFN-gamma. AC-splenic CD4(+), CD8(+), CD4(-)/CD8( -) (DN) T cells differentially suppressed antigen-induced proliferation and IFN-gamma production by immunized lymph node cells by a mechanism dependent on IL-10 and antigen. Cultures of lymph node cells, antigen, and AC-splenic T cells contained increased amounts of IL-10 and/orTGFbeta2. CONCLUSIONS: The differential, cytokine-dependent immunoregulatory effects of CD4( +) and CD8(+) AC-spleen cells observed in vitro parallel their effects in vivo. We suggest that the suppression of antigen-induced lymphocyte proliferation and IFN-gamma production by AC-spleen cells provides a useful in-vitro assay of the immunoregulatory activity of cell populations that are induced by the injection of antigen into the anterior chamber.
机译:目的:表征通过前房内注射抗原(AC-脾细胞)激活的脾细胞的体外免疫调节机制。方法:通过与TNP-BSA和AC脾脏共培养淋巴结细胞,量化AC脾细胞对TNP-BSA免疫小鼠的淋巴结细胞体外抗原诱导的增殖和干扰素γ产生的调节前房内TNP-BSA诱导的细胞。通过ELISA定量细胞因子的产生。结果:AC脾细胞产生的IL-4和IL-10明显高于TNP-BSA免疫小鼠或幼稚脾细胞产生的IL-4和IL-10。与来自免疫小鼠的脾细胞不同,交流脾细胞不产生IFN-γ。 AC脾CD4(+),CD8(+),CD4(-)/ CD8(-)(DN)T细胞通过依赖于IL-的机制差异性抑制抗原诱导的增殖和免疫淋巴结细胞产生的IFN-γ。 10和抗原。淋巴结细胞,抗原和AC脾T细胞的培养物中IL-10和/或TGFbeta2的含量增加。结论:体外观察到的CD4(+)和CD8(+)AC脾细胞的差异,细胞因子依赖性免疫调节作用与其体内作用平行。我们建议抑制抗原诱导的淋巴细胞增殖和AC脾细胞产生的IFN-γ提供了有用的体外检测细胞群免疫调节活性的方法,该活性是通过向前房注射抗原诱导的。

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