Iitaka M, Aguayo J F, Iwatani Y, Row V V, Volpé R
Department of Medicine, Wellesley Hospital, University of Toronto, Ontario, Canada.
J Clin Endocrinol Metab. 1988 Apr;66(4):708-14. doi: 10.1210/jcem-66-4-708.
The suppressor function in CD8 (suppressor/cytotoxic) T lymphocytes from patients with autoimmune thyroid disease and normal subjects has been studied. CD8 and CD4 (helper/inducer) cells were separated by the panning method. Patient's non-T cells and autologous CD4 cells were cultured with or without autologous or allogeneic CD8 cells in the presence of either pokeweed mitogen or Staphylococcus aureus strain Cowan 1 plus human thyroid microsomal antigen. Antithyroid microsomal antibody (AMA) and total immunoglobulin G (IgG)-secreting non-T cells were measured by enzyme-linked immunosorbent spot assay. With pokeweed mitogen stimulation, the suppressor effect of CD8 cells from patients with serum AMA on the induction of AMA (of IgG type)-secreting cells was significantly less than that of CD8 cells from normal subjects. CD8 cells from patients with no serum AMA suppressed the induction of AMA-secreting cells as much as did normal CD8 cells. CD8 cells from both patients and normal subjects suppressed the induction of IgG-secreting cells equally well. On the other hand, with the combination of S. aureus strain Cowan 1 and human thyroid microsomal antigen (1 mg/L) stimulation, CD8 cells from both normal subjects and patients only slightly suppressed the induction of IgG-secreting cells. However, under these circumstances, once again, CD8 cells from both normal subjects and patients with no serum AMA suppressed the induction of AMA-secreting cells, whereas CD8 cells from patients with serum AMA suppressed the induction of the AMA-secreting cells significantly less. Higher TMc concentrations enhanced the suppressor effect of CD8 cells from patients with serum AMA on the induction of AMA-secreting cells. Furthermore, Concanavalin A, when added to the stimuli described above, further inhibited the induction of both AMA- and IgG-secreting cells by CD8 cells from patients with serum AMA. There thus appears to be a relative defect of antigen-specific suppressor T lymphocyte function in CD8 cells from patients with autoimmune thyroid disease, which may result in the presence of autoantibody-secreting cells in those patients.
对自身免疫性甲状腺疾病患者及正常受试者的CD8(抑制/细胞毒性)T淋巴细胞的抑制功能进行了研究。通过淘选法分离CD8和CD4(辅助/诱导)细胞。将患者的非T细胞和自体CD4细胞与自体或异体CD8细胞一起培养,培养时加入或不加入商陆有丝分裂原或金黄色葡萄球菌考恩1株加人甲状腺微粒体抗原。通过酶联免疫吸附斑点试验检测抗甲状腺微粒体抗体(AMA)和分泌总免疫球蛋白G(IgG)的非T细胞。在商陆有丝分裂原刺激下,血清AMA阳性患者的CD8细胞对AMA(IgG型)分泌细胞诱导的抑制作用明显低于正常受试者的CD8细胞。无血清AMA患者的CD8细胞对AMA分泌细胞诱导的抑制作用与正常CD8细胞相同。患者和正常受试者的CD8细胞对IgG分泌细胞诱导的抑制作用同样良好。另一方面,在金黄色葡萄球菌考恩1株与人甲状腺微粒体抗原(1mg/L)联合刺激下,正常受试者和患者的CD8细胞仅轻微抑制IgG分泌细胞的诱导。然而,在这些情况下,同样,无血清AMA的正常受试者和患者的CD8细胞抑制AMA分泌细胞的诱导,而血清AMA阳性患者的CD8细胞对AMA分泌细胞诱导的抑制作用明显较弱。较高的甲状腺微粒体浓度增强了血清AMA阳性患者的CD8细胞对AMA分泌细胞诱导的抑制作用。此外,当将伴刀豆球蛋白A添加到上述刺激物中时,其进一步抑制了血清AMA阳性患者的CD8细胞对AMA和IgG分泌细胞的诱导。因此,自身免疫性甲状腺疾病患者的CD8细胞中似乎存在抗原特异性抑制性T淋巴细胞功能的相对缺陷,这可能导致这些患者中存在自身抗体分泌细胞。