131I治疗结节性甲状腺肿和32P治疗真性红细胞增多症后血淋巴细胞亚群及其功能的变化

J Wasserman, H Blomgren, B Petrini, E Svedmyr, P O Schnell, G Lundell, L V Von Stedingk
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引用次数: 5

摘要

本文对34例经131I治疗中毒性或中毒性甲状腺结节的患者进行了血液淋巴细胞群的检测。每隔一周给药一至三剂300-550 MBq的131I。淋巴细胞计数在治疗后1周和6周均明显减少。这种减少伴随着淋巴细胞亚群组成的改变。在给药后1周和6周,表达C'3膜受体(eac -玫瑰花结形成细胞)的淋巴细胞频率显著降低。在6周时,通过Leu 1单克隆抗体鉴定的T细胞频率有一个小的但有统计学意义的增加。这主要是由于辅助/诱导剂T细胞的比例增加,由Leu 3单克隆鉴定。131I处理也降低了欧陆有丝分裂原(PWM)刺激下淋巴细胞分泌免疫球蛋白(Ig)的能力。IgM的效果最大。IgG和IgA的分泌减少较少。植物血凝素(PHA)和豆豆蛋白A对淋巴细胞有丝分裂的刺激作用无明显变化。结论是,这些发现,除了有丝分裂原反应性,在很大程度上与癌症外部放射治疗后发生的情况相似。提示通过连续照射腺体的血淋巴细胞主要受到-射线的损伤。本文观察了32P对真性红细胞增多症16例患者外周血淋巴细胞群的影响。治疗前淋巴细胞计数在正常范围内,但通过抗总T细胞(Leu 1和4)、辅助/诱导剂(Leu 3)和抑制/细胞毒性T细胞(Leu 2)的单克隆抗体鉴定,某些膜结构的表达略有下降。此外,淋巴细胞对PHA和pwm诱导的Ig分泌的有丝分裂反应受到损害。单次口服32P (150-305 MBq)后,红细胞和/或血小板的产生正常化,治疗12周后血液淋巴细胞计数减少约40%。亚群检测显示,B1单克隆抗体鉴定的b细胞比例相对下降幅度最大。另一方面,表达上述T细胞标记物的淋巴细胞有所增加。32P处理显著提高了PHA反应性,但进一步降低了pwm诱导的Ig分泌。后一种观察结果与治疗后血清Ig浓度降低的发现一致。
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Changes of the blood lymphocyte subpopulations and their functions following 131I treatment for nodular goitre and 32P treatment for polycythemia vera.

The blood lymphocyte population was examined in 34 patients who were treated with 131I for toxic or atoxic nodular goitre. One to three doses of 300-550 MBq of 131I were administered at 1-week intervals. Lymphocyte counts were found to be significantly reduced at both 1 and 6 weeks after treatment. This decrease was accompanied by a changed composition of the lymphocyte subpopulations. The frequency of lymphocytes expressing membrane receptors for C'3 (EAC-rosette forming cells) was significantly reduced at 1 and 6 weeks following 131I administration. At 6 weeks there was a small but statistically significant increase of the frequency of T cells as identified by Leu 1 monoclonal antibodies. This was essentially due to an increased proportion of helper/inducer T cells as identified by Leu 3 monoclonals. 131I treatment also decreased the capacity of lymphocytes to secrete immunoglobulins (Ig) when stimulated with pokeweed mitogen (PWM). The greatest effect was observed for IgM. Secretion of IgG and IgA were less reduced. Mitogenic stimulations of lymphocytes with phytohemagglutinin (PHA) and concanavalin A were not significantly changed. It is concluded that these findings, with the exception of mitogen reactivity, are largely similar to those occurring following external radiation therapy for cancer. It is suggested that blood lymphocytes passing through the continuously irradiated gland are damaged mainly by beta-rays. The effect of 32P treatment on the blood lymphocyte population was examined in 16 patients with polycythemia vera. Before treatment the lymphocyte counts were within the normal range but the expression of certain membrane structures, as identified by monoclonal antibodies against total T cells (Leu 1 and 4), helper/inducer (Leu 3) and suppressor/cytotoxic T cells (Leu 2), were slightly decreased. Moreover, mitogenic responses of the lymphocytes to PHA and PWM-induced Ig secretion were impaired. Following a single oral dose of 32P (150-305 MBq), which normalized the production of erythrocytes and/or platelets, the blood lymphocyte counts were reduced by approximately 40 per cent 12 weeks after treatment. Examination of subsets demonstrated that the proportion of B-cells, as identified by B1 monoclonal antibodies, was decreased by the highest relative extent. On the other hand, lymphocytes expressing the above-mentioned T cell markers were somewhat increased. 32P treatment markedly increased PHA reactivity but it further reduced PWM-induced Ig secretion. The latter observation was in agreement with the finding that serum concentrations of Ig were reduced after treatment.

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