Greineder D K, Shevach E M, Rosenthal A S
J Immunol. 1976 Oct;117(4):1261-6.
Inhibition by anti-Ia sera of guinea pig T lymphocyte proliferation induced by allogeneic macrophages (MLR) and NaIO4 or neuraminidase-galactose oxidase-treated macrophages has been investigated in order to identify the target cell upon which the antisera act. Anti-2 and anti-13 alloantisera were found to inhibit both MLR and aldehydeinduced T cell reactivity when directed against the specificity of the stimulatory macrophage. Little or no inhibition was observed when these antisera were directed against the T lymphocyte specificity when cultures were harvested at the time of peak proliferation. In addition, anti-2 serum was found to inhibit macrophage-lymphocyte rosett formation at 20 hr between neuraminidase-galactose oxidase-treated strain 2 macrophages and strain 13 lymphocytes. These findings demonstrate that inhibition of T cell proliferation can be produced by anti-Ia sera directed against the macrophage and raise the possibility that Ir gene products may function in part at the level of the macrophage.
为了确定抗血清作用的靶细胞,研究了豚鼠抗Ia血清对同种异体巨噬细胞(混合淋巴细胞反应,MLR)以及经高碘酸钠或神经氨酸酶-半乳糖氧化酶处理的巨噬细胞诱导的T淋巴细胞增殖的抑制作用。当抗2和抗13同种异体抗血清针对刺激巨噬细胞的特异性时,发现它们能抑制MLR和醛诱导的T细胞反应性。当在增殖高峰期收获培养物时,若这些抗血清针对T淋巴细胞特异性,则几乎没有观察到抑制作用。此外,发现抗2血清在神经氨酸酶-半乳糖氧化酶处理的2型巨噬细胞与13型淋巴细胞之间20小时时可抑制巨噬细胞-淋巴细胞玫瑰花结的形成。这些发现表明,针对巨噬细胞的抗Ia血清可产生T细胞增殖的抑制作用,并增加了Ir基因产物可能部分在巨噬细胞水平发挥作用的可能性。