Fischer A, König W
Medizinische Mikrobiologie und Immunologie, AG Infektabwehr, Bochum, Germany.
Immunology. 1991 Oct;74(2):228-33.
We studied the mechanisms of action leading to the glucocorticoid (GC)-induced synthesis of the immunoglobulins (IgE, G, A, M) by human peripheral blood mononuclear cells (PBMC). It is shown that the enhanced Ig synthesis of GC-stimulated PBMC is dependent on the presence of T cells and monocytes. After stimulation of purified B cells with GC only a slight enhancement of IgM could be detected. Inhibition studies with neutralizing anti-interleukin-4 (IL-4) and anti-IL-6 antibodies revealed that the GC-induced IgE synthesis of PBMC is not dependent on the presence of IL-4 or IL-6. Stimulation of membrane-separated and co-cultured cell fractions revealed that the GC-induced enhancement of IgA and IgM synthesis is mediated by T-cell derived soluble mediators. The GC-induced IgG and IgE synthesis is dependent upon contact of B cells with monocytes. Antibodies against LFA-1 and ICAM-1 are capable to suppress the GC-induced IgE and IgG synthesis of PBMC. Furthermore, the monocyte expression of lymphocyte function antigen-1 (LFA-1), intercellular adhesion molecule-1 (ICAM-1) and HLA-DR is modulated by GC stimulation.
我们研究了导致糖皮质激素(GC)诱导人外周血单核细胞(PBMC)合成免疫球蛋白(IgE、G、A、M)的作用机制。结果表明,GC刺激的PBMC增强的Ig合成依赖于T细胞和单核细胞的存在。仅用GC刺激纯化的B细胞后,只能检测到IgM略有增强。用中和抗白细胞介素-4(IL-4)和抗IL-6抗体进行的抑制研究表明,GC诱导的PBMC的IgE合成不依赖于IL-4或IL-6的存在。对膜分离和共培养细胞组分的刺激表明,GC诱导的IgA和IgM合成增强是由T细胞衍生的可溶性介质介导的。GC诱导的IgG和IgE合成依赖于B细胞与单核细胞的接触。抗淋巴细胞功能相关抗原-1(LFA-1)和细胞间黏附分子-1(ICAM-1)的抗体能够抑制GC诱导的PBMC的IgE和IgG合成。此外,GC刺激可调节单核细胞上淋巴细胞功能抗原-1(LFA-1)、细胞间黏附分子-1(ICAM-1)和人类白细胞抗原-DR(HLA-DR)的表达。