Schalch L, Rordorf-Adam C, Dasch J R, Jungi T W
Institute of Veterinary Virology, University of Berne, Switzerland.
Biochem Biophys Res Commun. 1991 Jan 31;174(2):885-91. doi: 10.1016/0006-291x(91)91500-c.
Mononuclear cells (MNC) stimulated either with lipopolysaccharide (LPS) or with surface-adsorbed IgG elaborated significant amounts of tumor necrosis factor (TNF) bioactivity, as well as immunoenzymatically detectable TNF-alpha and interleukin-1 beta. (IL1-beta). In contrast, IgG-stimulated cells released little IL1 bioactivity, but released an IL1 inhibitor, as determined by the thymocyte costimulatory assay (LAF assay). This inhibition was not due to an inhibitory effect of cyclooxygenase products, e.g. prostaglandin-E2 in the LAF assay. In contrast, antibodies against transforming growth factor type beta (TGF-beta), which is an important inhibitor of the LAF assay, augmented the LAF activity of supernatants from LPS-stimulated and IgG-stimulated MNC. Anti-TGF-beta-modulated LAF inhibition was enhanced by acid treatment of supernatants from mononuclear cells, but not of those from purified monocytes. Antibody blocking experiments point for the first time to a TGF-beta species other than type 1 as a monocyte-derived TGF-beta activity. Thus, TGF-beta released in active form from monocytes may be the more important antagonist of IL1 than cyclooxygenase-derived mediators. It implies that the LAF assay, in the absence of anti-TGF-beta antibodies, is an inadequate indicator of IL1 activity.
用脂多糖（LPS）或表面吸附的IgG刺激的单核细胞（MNC）可产生大量肿瘤坏死因子（TNF）生物活性，以及免疫酶法可检测到的TNF-α和白细胞介素-1β（IL1-β）。相比之下，IgG刺激的细胞释放的IL1生物活性很少，但释放了一种IL1抑制剂，这是通过胸腺细胞共刺激试验（LAF试验）确定的。这种抑制作用不是由于环氧合酶产物的抑制作用，例如LAF试验中的前列腺素-E2。相反，针对转化生长因子β型（TGF-β）的抗体（TGF-β是LAF试验的重要抑制剂）增强了LPS刺激和IgG刺激的MNC上清液的LAF活性。抗TGF-β调节的LAF抑制作用通过对单核细胞上清液进行酸处理而增强，但对纯化单核细胞的上清液进行酸处理则没有增强。抗体阻断实验首次指出除1型以外的一种TGF-β作为单核细胞衍生的TGF-β活性。因此，从单核细胞以活性形式释放的TGF-β可能是比环氧合酶衍生介质更重要的IL1拮抗剂。这意味着在没有抗TGF-β抗体的情况下，LAF试验是IL1活性的不充分指标。
