Hirose A, Ikejima T, Gill D M
Infect Immun. 1985 Dec;50(3):765-70. doi: 10.1128/iai.50.3.765-770.1985.
Toxic shock syndrome toxin is already known to induce the production of interleukin-1 (IL-1) by preparations of monocytes and macrophages that are presumably contaminated with other types of cells. The response is enhanced by increasing the density of such monocytes, suggesting that the monocyte's response to toxic shock syndrome toxin may be augmented by its interaction with some other cell. Nevertheless, we now show that several human and murine macrophagelike cell lines (U937, J774, P388D1, and WEHI 3) produce IL-1 when exposed to toxic shock syndrome toxin, and therefore the basic response does not require the presence of cells of other lineages. The cultured cells generally produce less IL-1 than do monocytes, but considerably more IL-1 is induced from cells that have undergone a terminal differentiation as a result of exposure to 1 alpha,25-dihydroxyvitamin D3. High concentrations of cultured cels suppress the production of IL-1; this effect is apparently not due to long-lived inhibitors of IL-1 production or of IL-1 activity, but may be due to a short-lived inhibitor of production.
毒性休克综合征毒素已知可诱导单核细胞和巨噬细胞制剂产生白细胞介素-1(IL-1),这些制剂可能被其他类型的细胞污染。通过增加此类单核细胞的密度可增强这种反应,这表明单核细胞对毒性休克综合征毒素的反应可能会因其与其他某种细胞的相互作用而增强。然而,我们现在表明,几种人和小鼠的巨噬细胞样细胞系(U937、J774、P388D1和WEHI 3)在暴露于毒性休克综合征毒素时会产生IL-1,因此基本反应并不需要其他谱系的细胞存在。培养的细胞通常比单核细胞产生的IL-1少,但由于暴露于1α,25-二羟基维生素D3而经历终末分化的细胞可诱导产生更多的IL-1。高浓度的培养细胞会抑制IL-1的产生;这种效应显然不是由于IL-1产生或IL-1活性的长效抑制剂,而是可能由于一种产生的短效抑制剂。