Peterson K E, Braley-Mullen H
Department of Molecular Microbiology and Immunology, University of Missouri, Columbia 65212, USA.
Cell Immunol. 1995 Nov;166(1):123-30. doi: 10.1006/cimm.1995.0014.
Experimental autoimmune thyroiditis (EAT) induced by the transfer of mouse thyroglobulin (MTg)-immunized spleen cells, activated in vitro with MTg, can be suppressed by oral administration of PTg to donor mice prior to immunization. Oral administration of 1 mg PTg five times over a 10-day period before immunization with MTg-LPS resulted in reduced EAT severity in recipient mice compared with recipients of cells from saline-fed immunized donors. MTg- or PTg-specific proliferative responses were not decreased in PTg-fed donors and anti-MTg antibody was not decreased in the donor mice fed 1 mg PTg. However, anti-MTg antibody production was markedly decreased in recipients of cells from PTg-fed donors compared with recipients of control cells. IgG1, IgG2A, and IgG2B anti-MTg antibody responses were all suppressed by PTg feeding suggesting that tolerance may be induced in both Th1 and Th2 cells. The more severe and histologically distinct granulomatous form of EAT was also suppressed by feeding PTg to donor mice. Studies are underway to determine the mechanism of oral tolerance in this model.
通过转移经小鼠甲状腺球蛋白（MTg）免疫且在体外经MTg激活的脾细胞诱导的实验性自身免疫性甲状腺炎（EAT），可在免疫前对供体小鼠口服PTg来加以抑制。在用MTg-LPS免疫前的10天内，口服1毫克PTg五次，与接受来自用盐水喂养的免疫供体的细胞的受体小鼠相比，接受细胞的受体小鼠的EAT严重程度降低。在喂食PTg的供体中，MTg或PTg特异性增殖反应并未降低，且在喂食1毫克PTg的供体小鼠中，抗MTg抗体也未减少。然而，与接受对照细胞的受体相比，接受来自喂食PTg的供体的细胞的受体中抗MTg抗体的产生明显减少。PTg喂养可抑制IgG1、IgG2A和IgG2B抗MTg抗体反应，这表明Th1和Th2细胞中可能都诱导了耐受性。通过给供体小鼠喂食PTg，EAT更严重且组织学上不同的肉芽肿形式也受到抑制。目前正在进行研究以确定该模型中口服耐受性的机制。
