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甲状腺自身抗体合成调控的体外研究

In vitro studies on the control of thyroid autoantibody synthesis.

作者信息

McLachlan S M, Wee S L, McGregor A M, Smith B R, Hall R

出版信息

J Clin Lab Immunol. 1980 Jan;3(1):15-21.

PMID:6892932
Abstract

A current hypothesis suggests that autoimmune responses are prevented in normal individuals by a population of suppressor cells. We have investigated this using a system in which thyroid autoantibodies are synthesised in culture by peripheral blood mononuclear cells (PBM) from patients with Hashimoto's thyroiditis. A group of 8 Hashimoto patients and 17 normal subjects were used in the study. PBM from the group of patients did not differ significantly from those of the control group in terms of their ability to synthesise IgG in culture, to respond to allogeneic cells or to PHA. (Nor were any genetic differences observed between the two groups in terms of HLA-A, B or C antigens.) In 6 co-culture experiments involving equal numbers of PBM from patients and normal donors, inhibition of thyroid antibody production was not observed. Additionally, T-cell enriched populations from 2 normal donors were unable to specifically inhibit thyroid antibody synthesis by Hashimoto B-cell enriched fractions from 2 Hashimoto patients. Consequently, we were unable to show suppressor cell activity in normal PBM and it is suggested that these cells may need to be activated by antigen before their presence can be demonstrated.

摘要

目前的一种假说认为,正常个体中的自身免疫反应是由一群抑制性细胞所阻止的。我们利用一种系统对此进行了研究,在该系统中,桥本甲状腺炎患者外周血单个核细胞(PBM)在培养中合成甲状腺自身抗体。本研究使用了一组8名桥本患者和17名正常受试者。患者组的PBM在培养中合成IgG的能力、对同种异体细胞或PHA的反应方面,与对照组并无显著差异。(两组在HLA - A、B或C抗原方面也未观察到任何基因差异。)在涉及等量患者和正常供体PBM的6项共培养实验中,未观察到甲状腺抗体产生受到抑制。此外,来自2名正常供体的富含T细胞群体,无法特异性抑制来自2名桥本患者的富含B细胞的桥本甲状腺炎组分合成甲状腺抗体。因此,我们无法在正常PBM中显示抑制性细胞活性,提示这些细胞可能需要被抗原激活后才能显示其存在。

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