卵清蛋白TCR转基因小鼠中的高剂量口服耐受:IL-12的全身中和增强TGF-β分泌和T细胞凋亡。
High dose oral tolerance in ovalbumin TCR-transgenic mice: systemic neutralization of IL-12 augments TGF-beta secretion and T cell apoptosis.
作者信息
Marth T, Strober W, Kelsall B L
机构信息
Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.
出版信息
J Immunol. 1996 Sep 15;157(6):2348-57.
The immune response to oral Ag administration, including the development of oral tolerance, was explored with the use of OVA TCR-transgenic mice. Feeding high doses of OVA enhanced IFN-gamma production in the Peyer's patches, but induced tolerance in the peripheral lymphoid tissues marked by suppressed proliferative and cytokine responses. Systemic administration of Abs to IL-12 (anti-IL-12) simultaneous with Ag feeding modestly enhanced the degree of tolerance in the peripheral lymphoid tissues, as shown by increased suppression of proliferative responses after in vitro restimulation, and secondary responses in the popliteal lymph nodes following in vivo challenge and in vitro restimulation. Systemic anti-IL-12 treatment was associated with augmented TGF-beta production and T cell apoptosis in both Peyer's patches and peripheral lymphoid tissues. Cell mixing studies and proliferation assays in the presence of anti-TGF-beta provided evidence that the increased suppression of responses induced by anti-IL-12 was due primarily to the secretion of TGF-beta. These findings suggest that IL-12 negatively regulates two of the main mechanisms of oral tolerance, TGF-beta production and clonal deletion via apoptosis. in addition, they suggest that the combination of oral Ag feeding and systemic anti-IL-12 administration may be of benefit in the treatment of autoimmune diseases.
利用卵清蛋白(OVA)T细胞受体转基因小鼠,研究了口服抗原(Ag)后的免疫反应,包括口服耐受的形成。喂食高剂量的OVA可增强派尔集合淋巴结中γ干扰素的产生,但会在外周淋巴组织中诱导耐受,其特征为增殖反应和细胞因子反应受到抑制。在喂食抗原的同时全身给予抗白细胞介素12(IL-12)抗体(抗IL-12),适度增强了外周淋巴组织中的耐受程度,体外再刺激后增殖反应的抑制增强以及体内攻击和体外再刺激后腘窝淋巴结中的二次反应均表明了这一点。全身抗IL-12治疗与派尔集合淋巴结和外周淋巴组织中转化生长因子β(TGF-β)产生增加及T细胞凋亡有关。细胞混合研究和在抗TGF-β存在下的增殖试验提供了证据,表明抗IL-12诱导的反应抑制增强主要是由于TGF-β的分泌。这些发现表明,IL-12负向调节口服耐受的两个主要机制,即TGF-β产生和通过凋亡进行的克隆清除。此外,这些发现还表明,口服抗原喂食和全身抗IL-12给药相结合可能对自身免疫性疾病的治疗有益。