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首页> 外文期刊>The journal of immunology >Heavy chain-specific suppression of immunoglobulin synthesis and secretion by lymphocytes from patients with selective IgA deficiency.
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Heavy chain-specific suppression of immunoglobulin synthesis and secretion by lymphocytes from patients with selective IgA deficiency.

机译:重链特异性抑制免疫球蛋白合成和分泌的选择性IgA缺乏症患者的淋巴细胞。

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A simple, solid-state immunofluorescent assay specific for the heavy chain of human immunoglobulins (Ig) was adapted for studying pokeweed mitogen- (PWM) stimulated Ig biosynthesis and secretion by peripheral blood lymphocytes (PBL) in vitro. PBL from patients with panhypogammaglobulinemia were noted to synthesize and secrete decreased amounts of all classes of immunoglobulin after polyclonal activation of B cells in vitro with PWM. PBL from 14 patients with selective deficiency of IgA were capable of synthesizing and secreting significant levels of IgG and IgM after culture with PWM; however, they did not produce appreciable amounts of IgA. Thus, B lymphocyte differentiation in vitro parallels the clinical status. Several different immunoregulatory phenomena were observed when PBL from patients with selective IgA deficiency were co-cultivated with cells from healthy donors. Most notable was the specific suppression of IgA synthesis and secretion seen in 8 of 14 patients studied, although other modulatory effects including enhancement and suppression of all Ig classes were also observed. These results suggest that the pathologic basis of selective IgA deficiency may be heterogeneous and support a model for the role of Ig class-specific suppressor cells in the pathogenesis of some cases of selective IgA deficiency.
机译:一种适用于人免疫球蛋白(Ig)重链的简单,固态免疫荧光测定方法,适用于研究商陆有丝分裂原(PWM)刺激的Ig生物合成和外周血淋巴细胞(PBL)分泌。在体外用PWM多克隆激活B细胞后,来自全血球蛋白球蛋白血症患者的PBL被发现合成并分泌减少量的所有类别的免疫球蛋白。 14名患有选择性IgA缺乏症的患者的PBL在PWM培养后能够合成并分泌大量的IgG和IgM。然而,它们没有产生可观的IgA。因此,体外B淋巴细胞分化与临床状况相符。将选择性IgA缺乏症患者的PBL与健康供体的细胞共培养时,观察到几种不同的免疫调节现象。最值得注意的是在研究的14位患者中有8位患者特异性抑制了IgA合成和分泌,尽管还观察到其他调节作用,包括增强和抑制所有Ig类。这些结果表明选择性IgA缺乏症的病理基础可能是异质的,并支持了Ig类特异性抑制细胞在某些选择性IgA缺乏症的发病机理中的作用模型。

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