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通过酶联免疫斑点(ELISPOT)技术对产生IgA的细胞进行计数,以评估柳氮磺胺吡啶对炎性关节炎的作用。

Enumeration of IgA producing cells by the enzyme linked immunospot (ELISPOT) technique to evaluate sulphasalazine effects in inflammatory arthritides.

作者信息

Feltelius N, Gudmundsson S, Wennersten L, Sjöberg O, Hällgren R, Klareskog L

机构信息

Department of Internal Medicine, Uppsala University Hospital, Sweden.

出版信息

Ann Rheum Dis. 1991 Jun;50(6):369-71. doi: 10.1136/ard.50.6.369.

Abstract

Numbers of IgA producing cells in peripheral blood were determined by the enzyme linked immunospot (ELISPOT) technique in 15 patients with inflammatory arthritides receiving sulphasalazine treatment. The numbers of IgA producing cells decreased significantly after the first three weeks of treatment. In 11 of the patients this decrease persisted, whereas a subsequent increase was seen in the four others; in two of these latter patients this increase coincided with a temporary withdrawal of the sulphasalazine treatment. A reduction of serum concentrations of IgA and haptoglobin was seen after three months' treatment. Eleven of the patients had a subjective improvement in their joint disease during the first three months of treatment. Analysis of circulating cells committed for IgA secretion may constitute one way of assessing gut associated immunity indirectly, and the present data suggest that sulphasalazine has a rapid effect on lymphocytes possibly originating from the gut and that such an effect precedes improvement in laboratory parameters and clinical symptoms in arthritic diseases.

摘要

采用酶联免疫斑点(ELISPOT)技术测定了15例接受柳氮磺胺吡啶治疗的炎性关节炎患者外周血中产生IgA的细胞数量。治疗前三周后,产生IgA的细胞数量显著减少。11例患者的这种减少持续存在,而另外4例患者随后出现增加;在这4例患者中的2例,这种增加与柳氮磺胺吡啶治疗的暂时中断同时出现。治疗三个月后,血清IgA和触珠蛋白浓度降低。11例患者在治疗的前三个月关节疾病有主观改善。分析循环中致力于IgA分泌的细胞可能构成间接评估肠道相关免疫的一种方法,目前的数据表明柳氮磺胺吡啶对可能源自肠道的淋巴细胞有快速作用,并且这种作用在关节炎疾病的实验室参数和临床症状改善之前出现。

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本文引用的文献

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Histopathology of intestinal inflammation related to reactive arthritis.
Gut. 1987 Apr;28(4):394-401. doi: 10.1136/gut.28.4.394.
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Preliminary evidence for gut involvement in the pathogenesis of rheumatoid arthritis?
Br J Rheumatol. 1986 May;25(2):162-6. doi: 10.1093/rheumatology/25.2.162.

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