Ilfeld D, Kuperman O
Clin Exp Immunol. 1982 Oct;50(1):99-106.
We have previously reported that three patients with familial Mediterranean fever (FMF) had deficient concanavalin A (Con A) activated suppressor cell inhibition of the proliferation of healthy volunteers' phytohaemagglutinin stimulated responder cells. When these three FMF patients were treated with long term oral colchicine (2 mg/day), their Con A activated suppressor cell deficiency was corrected and FMF attacks prevented. In the present report, the effect of as well as colchicine treatment on the suppressor cell function of these three FMF patients as well as one more FMF patient was tested to determine whether colchicine can directly increase suppressor cell function rather than colchicine's preventing FMF attacks by unknown mechanisms which only indirectly results in a correction of the suppressor cell deficiency. Long term oral colchicine treatment corrected the suppressor cell deficiency in the four FMF patients (5±2%, 35±5%, and 46±4% for mean ±s.e.m.% suppression for 0, 1 and 2 mg/day of oral colchicine, respectively). Oral colchicine treatment corrected their suppressor cell deficiency within one week of commencing treatment and even corrected one of the FMF patient's suppressor cell deficiency while he still had some FMF attacks on 1 mg/day of colchicine. Suppressor cells from two of the untreated FMF patients cultured with 10 M colchicine plus Con A significantly (<0·01) suppressed proliferation (36±5%) as compared to their suppressor cells cultured only with Con A (4±7%). Furthermore, these untreated FMF patients' suppressor cells cultured with 10 M colchicine (without Con A) often suppressed as compared to their suppressor cells cultured in medium. Thus colchicine appears to directly correct these FMF patients' suppressor cell deficiency. These observations raise the possibility that colchicine may be therapeutically useful in treating patients with other diseases associated with an absolute or relative deficiency of suppressor cell function.
我们之前报道过，三名家族性地中海热（FMF）患者的伴刀豆球蛋白A（Con A）激活的抑制细胞对健康志愿者的植物血凝素刺激的反应细胞增殖的抑制作用不足。当这三名FMF患者接受长期口服秋水仙碱（2毫克/天）治疗时，他们的Con A激活的抑制细胞缺陷得到纠正，FMF发作得到预防。在本报告中，测试了秋水仙碱治疗以及对这三名FMF患者和另一名FMF患者的抑制细胞功能的影响，以确定秋水仙碱是否能直接增强抑制细胞功能，而不是秋水仙碱通过未知机制预防FMF发作，而这种机制只是间接导致抑制细胞缺陷的纠正。长期口服秋水仙碱治疗纠正了四名FMF患者的抑制细胞缺陷（口服秋水仙碱0、1和2毫克/天的平均±标准误抑制率分别为5±2%、35±5%和46±4%）。口服秋水仙碱治疗在开始治疗的一周内纠正了他们的抑制细胞缺陷，甚至在一名FMF患者每天服用1毫克秋水仙碱仍有一些FMF发作时，也纠正了他的抑制细胞缺陷。与仅用Con A培养的抑制细胞（4±7%）相比，用10μM秋水仙碱加Con A培养的两名未治疗的FMF患者的抑制细胞显著（<0·）抑制增殖（36±5%）。此外，与在培养基中培养的抑制细胞相比，用10μM秋水仙碱（无Con A）培养的这些未治疗的FMF患者的抑制细胞常常有抑制作用。因此，秋水仙碱似乎能直接纠正这些FMF患者的抑制细胞缺陷。这些观察结果增加了秋水仙碱在治疗其他与抑制细胞功能绝对或相对缺陷相关疾病的患者中可能具有治疗作用的可能性。
