Kou K, Kawano Y, Yoshizawa I, Noma T
Department of Pediatrics, Saitama Medical School.
Arerugi. 1994 Mar;43(3):482-91.
As with normal lymphocytes, small amounts of interferon-gamma (IFN-gamma) were spontaneously produced by lymphocytes from patients with bronchial asthma, and this bronchial asthma, and this production was markedly enhanced by concanavalin A (Con A) stimulation. Distinct from normal lymphocytes, however, IFN-gamma synthesis from patients' lymphocytes decreased in a dose dependent manner on stimulation with Dermatophagoides farinae (Df) antigen. IFN-gamma-producing cells are defined as being of the CD4+ 45RO+ T cell subset, which failed to produce IFN-gamma in Df-stimulated patients' lymphocytes. As the decreased production of IFN-gamma by antigenic stimulation was exclusively induced by Df antigen, but not by ovalbumin (OVA) or Japanese cedar (JC) antigen, it is concluded that Df antigen specifically suppressed IFN-gamma production in patients' lymphocytes. The IFN-gamma synthesis from normal lymphocytes was suppressed by the addition of IL-4 in a dose dependent manner. Moreover, anti-IL-4 antibody dose dependently enhanced IFN-gamma production from Df-stimulated patients' lymphocytes but not from unstimulated lymphocytes. These results indicate that IFN-gamma production by patients' lymphocytes is suppressed by the endogenous IL-4. Reduced IFN-gamma production in patients' lymphocytes on stimulation with Df antigen may lead to the overproduction of IgE in vivo.
与正常淋巴细胞一样，支气管哮喘患者的淋巴细胞会自发产生少量干扰素-γ（IFN-γ），且这种产生在伴刀豆球蛋白A（Con A）刺激下会显著增强。然而，与正常淋巴细胞不同的是，患者淋巴细胞经粉尘螨（Df）抗原刺激后，IFN-γ合成呈剂量依赖性降低。产生IFN-γ的细胞被定义为CD4 + 45RO + T细胞亚群，在Df刺激的患者淋巴细胞中该亚群无法产生IFN-γ。由于抗原刺激导致的IFN-γ产生减少仅由Df抗原诱导，而非由卵清蛋白（OVA）或日本雪松（JC）抗原诱导，因此得出结论，Df抗原特异性抑制患者淋巴细胞中IFN-γ的产生。正常淋巴细胞的IFN-γ合成会因添加IL-4而呈剂量依赖性受到抑制。此外，抗IL-4抗体呈剂量依赖性增强Df刺激的患者淋巴细胞而非未刺激淋巴细胞的IFN-γ产生。这些结果表明，患者淋巴细胞产生的IFN-γ受到内源性IL-4的抑制。患者淋巴细胞经Df抗原刺激后IFN-γ产生减少可能导致体内IgE产生过多。
