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口服秋水仙碱对哮喘患者T细胞亚群、单核细胞及伴刀豆球蛋白A诱导的抑制细胞功能的影响。

Effect of oral colchicine on T cell subsets, monocytes and concanavalin A-induced suppressor cell function in asthmatic patients.

作者信息

Ilfeld D N, Mazar A, Garty M, Fink G, Spitzer S, Pecht M, Netzer L, Trainin N, Kuperman O

出版信息

Clin Allergy. 1986 Sep;16(5):407-16. doi: 10.1111/j.1365-2222.1986.tb01975.x.

Abstract

Asthmatic patients have a deficiency of concanavalin A-(Con A) induced suppressor cell function. We tested whether oral colchicine 0.5 mg twice daily for 7 days could correct this immunoregulatory abnormality. Peripheral blood mononuclear cells were incubated with Con A and then suppression of proliferation was measured by coculture of these cells with healthy volunteers' mononuclear cells and phytohaemagglutinin. Sixteen asthmatic patients had significantly (P less than 0.002) decreased Con A-induced suppressor cell function (17.0 +/- 17.2%, mean +/- s.d.) as compared to 13 healthy volunteers (37.9 +/- 14.9%). Oral colchicine significantly (P less than 0.05) increased, though only partially corrected, these 16 asthmatic patients' Con A-induced suppressor cell function (28.1 +/- 14.3%). Asthmatic patients had an increased number of monocytes (691 +/- 289 vs 388 +/- 271/mm3 for normals, P less than 0.01) and a normal number of lymphocytes, Leu 4+ total T cells, Leu 3+ helper/inducer T cells, and Leu 2+ suppressor/cytotoxic T cells as well as a normal Leu 3/Leu 2 ratio. Oral colchicine significantly (P less than 0.005) decreased the number of monocytes (451 +/- 255/mm3) without significantly affecting the number of lymphocytes, Leu 4+, Leu 3+, or Leu 2+ T cells, or the Leu 3/Leu 2 ratio. These results are consistent with the hypothesis that the deficiency of Con A-induced suppressor cell function in asthmatic patients may be due, in part, to an increased number and/or abnormal activity of monocytes. If so, then oral colchicine may have partially corrected the deficiency of Con A-induced suppressor cell function by decreasing the number and/or modulating the activity of monocytes.

摘要

哮喘患者存在伴刀豆球蛋白A(Con A)诱导的抑制细胞功能缺陷。我们测试了每日两次口服0.5毫克秋水仙碱,持续7天是否能纠正这种免疫调节异常。将外周血单个核细胞与Con A一起孵育,然后通过将这些细胞与健康志愿者的单个核细胞及植物血凝素共同培养来测量增殖抑制情况。与13名健康志愿者(37.9±14.9%)相比,16名哮喘患者的Con A诱导的抑制细胞功能显著降低(P<0.002)(17.0±17.2%,均值±标准差)。口服秋水仙碱显著(P<0.05)提高了这16名哮喘患者的Con A诱导的抑制细胞功能(28.1±14.3%),尽管只是部分纠正。哮喘患者的单核细胞数量增加(正常人为388±271/mm³,哮喘患者为691±289/mm³,P<0.01),淋巴细胞、Leu 4⁺总T细胞、Leu 3⁺辅助/诱导T细胞、Leu 2⁺抑制/细胞毒性T细胞数量正常,Leu 3/Leu 2比值也正常。口服秋水仙碱显著(P<0.005)降低了单核细胞数量(451±255/mm³),而对淋巴细胞、Leu 4⁺、Leu 3⁺或Leu 2⁺T细胞数量以及Leu 3/Leu 2比值没有显著影响。这些结果与以下假设一致,即哮喘患者Con A诱导的抑制细胞功能缺陷可能部分归因于单核细胞数量增加和/或活性异常。如果是这样,那么口服秋水仙碱可能通过减少单核细胞数量和/或调节其活性部分纠正了Con A诱导的抑制细胞功能缺陷。

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