Lester M R, Hofer M F, Renz H, Trumble A E, Gelfand E W, Leung D Y
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206 USA.
Clin Immunol Immunopathol. 1995 Dec;77(3):332-8. doi: 10.1006/clin.1995.1160.
Atopic dermatitis (AD) is a chronic skin disorder associated with elevated serum IgE and colonization of the skin by Staphylococi which secrete toxins with superantigenic activity. The present study examined the immunomodulatory effects of toxic shock syndrome toxin (TSST)-1, a prototypic superantigen, on IgE synthesis by interleukin (IL)-4-stimulated peripheral blood mononuclear cells (PBMC) from five patients with AD and five normal subjects. TSST-1 inhibited IL-4-induced IgE synthesis by AD and normal PBMC (P < 0.05). In contrast, IgG synthesis was not similarly affected (P > 0.30). Inhibition of IL-4-induced IgE production was associated with induction of interferon (IFN)-gamma synthesis by TSST-1 (P < 0.02). Normal PBMC synthesized significantly more (P < 0.005) IFN-gamma than AD PBMC. A neutralizing antibody to IFN-gamma reversed TSST-1-induced suppression of IgE synthesis by the normal PBMC (P < 0.03), but not the AD PBMC. In AD, but not normal, PBMC anti-IFN-alpha antibody reversed the suppression of IgE synthesis induced by TSST-1. These results demonstrate that TSST-1 uses different mechanisms for modulation of IgE synthesis in AD versus normal PBMC. Furthermore, the reversal of TSST-1-induced suppression of IgE synthesis in AD PBMC by anti-IFN-alpha, but not anti-IFN-gamma, is consistent with the concept that AD is associated with defective Th1 cell function and enhanced monocyte activity.
特应性皮炎(AD)是一种慢性皮肤疾病,与血清IgE升高以及葡萄球菌在皮肤的定植有关,这些葡萄球菌分泌具有超抗原活性的毒素。本研究检测了毒性休克综合征毒素(TSST)-1(一种典型的超抗原)对5例AD患者和5名正常受试者经白细胞介素(IL)-4刺激的外周血单个核细胞(PBMC)合成IgE的免疫调节作用。TSST-1抑制AD患者和正常PBMC经IL-4诱导的IgE合成(P<0.05)。相比之下,IgG合成未受到类似影响(P>0.30)。TSST-1抑制IL-4诱导的IgE产生与诱导干扰素(IFN)-γ合成有关(P<0.02)。正常PBMC合成的IFN-γ显著多于AD患者的PBMC(P<0.005)。一种针对IFN-γ的中和抗体可逆转TSST-1对正常PBMC诱导的IgE合成的抑制作用(P<0.03),但对AD患者的PBMC无效。在AD患者的PBMC中,而非正常PBMC中,抗IFN-α抗体可逆转TSST-1诱导的IgE合成抑制作用。这些结果表明,TSST-1在AD患者和正常PBMC中调节IgE合成的机制不同。此外,抗IFN-α而非抗IFN-γ可逆转TSST-1对AD患者PBMC诱导的IgE合成抑制作用,这与AD与Th1细胞功能缺陷和单核细胞活性增强相关的概念一致。