Deficiency of the autologous mixed lymphocyte reaction in patients with primary biliary cirrhosis.
Deficiency of the autologous mixed lymphocyte reaction in patients with primary biliary cirrhosis.
复制标题
原发性胆汁性肝硬化患者自体混合淋巴细胞反应缺乏。
DOI：
10.1172/jci109982
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
W. Strober
中科院分区：
文献类型：
--
作者：
S. James;C. Elson;J. Waggoner;E. Jones;W. Strober
在这项研究中，我们发现原发性胆汁性肝硬化（PCB）患者产生自体混合淋巴细胞反应（AMLR）的能力明显不足，但产生同种异体混合淋巴细胞反应（MLR）的能力正常。这种缺陷不是由于增殖反应的时间过程的差异，也不是由于对刺激细胞数量变化的反应的改变。无论采用何种方法分离自体刺激细胞，都一致发现这种缺陷。从PBC患者获得的应答细胞和刺激细胞在异基因正常人血清中产生MLR的能力与正常细胞相似。此外，PBC患者的血清在相似程度上抑制了正常淋巴细胞产生AMLR和MLR的能力，这表明PBC中AMLR的缺陷不是由血清因素引起的。研究表明，AMLR中的应答细胞群包含介导抑制的细胞亚群。因此，AMLR的缺乏可能与先前描述的PBC患者抑制功能异常有关。
In this study we show that patients with primary biliary cirrhosis (PCB) have a marked deficiency in the ability to generate an autologous mixed lymphocyte reaction (AMLR) but have a normal ability to generate an allogeneic mixed lymphocyte reaction (MLR). This deficiency is not due to differences in the time-course of the proliferative response or to an altered response to variable numbers of stimulator cells. The deficiency was consistently found irrespective of the methods used to isolate autologous stimulator cells. Both responder cells and stimulator cells obtained from patients with PBC were similar to normal cells in their ability to generate an MLR in allogeneic normal human serum. In addition, serum from patients with PBC inhibited the ability of normal lymphocytes to generate both the AMLR and MLR to a similar degree, suggesting that the defect of the AMLR in PBC is not due to a serum factor. It has been shown that the responder cell population in the AMLR contains a subpopulation of cells that mediate suppression. Therefore, it is possible that the deficiency of the AMLR may be related to previously described abnormalities of suppressor function in patients with PBC.