Subpopulations of circulating B cells and regulatory T cells involved in in vitro immunoglobulin E production in atopic patients with elevted serum immunoglobulin E.

Subpopulations of circulating B cells and regulatory T cells involved in in vitro immunoglobulin E production in atopic patients with elevted serum immunoglobulin E.
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血清免疫球蛋白 E 升高的特应性患者中参与体外免疫球蛋白 E 产生的循环 B 细胞和调节性 T 细胞亚群。

DOI:
10.1172/jci109810
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发表时间:
1980
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Stevens,RH
Stevens,RH
中科院分区:
--
文献类型:
--
作者:
Saxon,A;Morrow,C;Stevens,RH

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被引文献

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研究了正常人和患有呼吸道变态反应、特应性皮炎和血清IgE水平明显升高(> 5,000 ng/ml)的特应性患者中产生免疫球蛋白(IG)E的B淋巴细胞亚群和调节这种IgE产生的调节性T细胞。将外周血淋巴细胞(PBL)分离成T和B细胞部分,并测定了B细胞在商陆有丝分裂原(PWM)和/或T细胞存在或不存在下产生IgE的能力。患者有一个循环细胞群,在没有T淋巴细胞和PWM的情况下,在体外自发产生高达6 ng的IgE(每4 × 10(5)个非E玫瑰花结细胞)。正常人外周血淋巴细胞不具有这种细胞。这种IgE合成主要发生在培养的前72小时(>75%)。在患者之间以及在重复的情况下研究的同一患者中,它们的活性范围很广(从<300到6,000 pg/培养物)。PWM(平均抑制率为37%)或正常T淋巴细胞(平均抑制率为42%)可抑制这种自发性IgE产生。在13个实验中的7个中,患者缺乏能够抑制这种自发IgE合成的T淋巴细胞。功能不同的B细胞被确定在患者和正常人,响应PWM与IgE的生产在体外和所需的T辅助细胞活性。患者具有正常的PWM响应性B细胞IgE生物合成活性和这些B细胞的辅助性T细胞功能。还评价了PWM驱动的IgE合成的抑制性T细胞活性。正常人和患者的T淋巴细胞对PWM驱动的IgE产生提供了相似水平的T细胞抑制功能。血清IgE升高的患者在其PBL中不存在抑制自发IgE产生的T淋巴细胞时具有这些抑制性T细胞。
The B lymphocyte subpopulations producing immunoglobulin (Ig)E and the regulatory T cells modulating this IgE production in normals, and in atopic patients with respiratory allergy, atopic dermatitis, and markedly elevated serum IgE levels (>5,000 ng/ml), were investigated. Peripheral blood lymphocytes (PBL) were separated into T and B cell fractions and the ability of B cells to produce IgE in the presence or absence of pokeweed mitogen (PWM) and/or T cells ws determined. The patients had a circulating population of cells which spontaneously produced up to 6 ng of IgE in vitro (per 4 X 10(5) non-E-rosetting cells) in the absence of T lymphocytes and PWM. PBL from normals did not possess such cells. This IgE synthesis occurred primarily (>75%) over the first 72 h of culture. There was a wide range in their activity between patients and from the same patient studied on repeated occasions (from <300 to 6,000 pg per culture). This spontaneous IgE production was inhibited by PWM (mean inhibition, 37%) or normal T lymphocytes (mean inhibition, 42%). The patients lacked T lymphocytes capable of inhibiting this spontaneous IgE synthesis in 7 of 13 experiments. Functionally distinct B cells were identified in the patients and normals that responded to PWM with IgE production in vitro and required T-helper cell activity. Patients had normal PWM-responsive B cell IgE biosynthetic activity and T-helper function for these B cells. Suppressor T cell activity for PWM-driven IgE synthesis was also evaluated. Both the normals' and the patients' T lymphocytes provided similar levels of T cell suppressor function for PWM-driven IgE production. Patients with elevated serum IgE possessed these inhibitory T cells at times when the T lymphocytes which suppressed spontaneous igE production were absent from their PBL.