Zimecki M, Kapp J A
Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław.
Arch Immunol Ther Exp (Warsz). 1994;42(5-6):361-7.
The purpose of this study was to investigate differences in T-B cell signalling between B cells from normal and immunodeficient mice. B cell blasts from normal and immunodeficient mice expressed comparable levels of membrane-associated IL-1. B cells from normal, but not immunodeficient mice, prefixed with glutaraldehyde and cultured with thymocytes or a T cell line BK33, induce in T cells production of a factor which causes release of IL-1 by macrophages. This factor, preincubated with B cells from immunodeficient mice significantly enhances their APC function. Furthermore, this cytokine induces expression of Lyb-5 alloantigen on B cells from immunodeficient mice. This effect could be blocked by neutralizing antibodies to IL-6 but not to IL-2, IL-4 or GM-CSF. We conclude that immature B cells from immunodeficient (CBA/N x BALB/c)F1 mice are unable to stimulate interacting T cells to produce IL-6 and therefore are inefficient antigen presenting cells.
本研究的目的是调查正常小鼠和免疫缺陷小鼠的B细胞之间T-B细胞信号传导的差异。正常小鼠和免疫缺陷小鼠的B细胞母细胞表达相当水平的膜相关白细胞介素-1(IL-1)。用戊二醛固定并与胸腺细胞或T细胞系BK33一起培养的正常小鼠而非免疫缺陷小鼠的B细胞,可诱导T细胞产生一种能使巨噬细胞释放IL-1的因子。该因子与免疫缺陷小鼠的B细胞预孵育后,可显著增强其抗原呈递细胞(APC)功能。此外,这种细胞因子可诱导免疫缺陷小鼠B细胞上Lyb-5同种抗原的表达。这种效应可被抗IL-6的中和抗体阻断,但不能被抗IL-2、IL-4或粒细胞-巨噬细胞集落刺激因子(GM-CSF)的中和抗体阻断。我们得出结论,免疫缺陷(CBA/N×BALB/c)F1小鼠的未成熟B细胞无法刺激相互作用的T细胞产生IL-6,因此是低效的抗原呈递细胞。