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环孢素A处理的小鼠中,抑制性T细胞可预防实验性红细胞自身免疫。

Experimental erythrocyte autoimmunity prevented by suppressor T cells in mice treated with Cyclosporin-A.

作者信息

Cox K O, Allison A C, Samcewicz B

出版信息

Clin Immunol Immunopathol. 1983 Jul;28(1):90-5. doi: 10.1016/0090-1229(83)90191-5.

DOI:10.1016/0090-1229(83)90191-5
PMID:6223763
Abstract

Mice injected with rat erythrocytes produce erythrocyte autoantibodies and suppressor cells that inhibit autoantibody production without inhibiting the net production of antibodies against rat RBC. Here it is shown that injecting mice with Cyclosporin-A daily for up to 13 days during the course of injections of rat RBC significantly inhibits autoantibody production. Antibody production against rat RBC was also inhibited. The Cyclosporin-A-treated mice that did not produce autoantibodies produced suppressor cells that inhibited autoantibody production in adoptive transfer experiments. These suppressor cells, which did not inhibit antibody production against rat RBC, were destroyed by treatment with anti-Thy 1.2 serum and complement. From the results, it is suggested that in this experimentally induced autoimmune disease, suppressor T cells may be activated and/or preferentially spared in Cyclosporin-A-treated mice.

摘要

注射大鼠红细胞的小鼠会产生红细胞自身抗体和抑制细胞,这些抑制细胞可抑制自身抗体的产生,而不抑制针对大鼠红细胞的抗体的净产生。本文表明,在注射大鼠红细胞的过程中,每天给小鼠注射环孢素A,持续13天,可显著抑制自身抗体的产生。针对大鼠红细胞的抗体产生也受到抑制。在过继转移实验中,未产生自身抗体的经环孢素A处理的小鼠产生了抑制自身抗体产生的抑制细胞。这些不抑制针对大鼠红细胞的抗体产生的抑制细胞,在用抗Thy 1.2血清和补体处理后被破坏。从结果来看,提示在这种实验性诱导的自身免疫性疾病中,抑制性T细胞可能在经环孢素A处理的小鼠中被激活和/或优先得以保留。

相似文献

1
Experimental erythrocyte autoimmunity prevented by suppressor T cells in mice treated with Cyclosporin-A.环孢素A处理的小鼠中,抑制性T细胞可预防实验性红细胞自身免疫。
Clin Immunol Immunopathol. 1983 Jul;28(1):90-5. doi: 10.1016/0090-1229(83)90191-5.
2
Experimental erythrocyte autoantibodies. V. Induction and suppression of red blood cell autoantibodies in mice injected with rat bromelain-treated red blood cells.实验性红细胞自身抗体。V. 注射经大鼠菠萝蛋白酶处理的红细胞的小鼠中红细胞自身抗体的诱导与抑制
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Effects of cyclosporin A on the production of experimental anti-erythrocyte autoantibodies in mice.环孢素A对小鼠实验性抗红细胞自身抗体产生的影响。
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Int Arch Allergy Appl Immunol. 1984;73(1):89-91.
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Experimental erythrocyte autoimmunity. II. Autoantibody-specific suppressor cells present in blood.实验性红细胞自身免疫。II. 血液中存在的自身抗体特异性抑制细胞。
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Experimental erythrocyte autoimmunity. Specificity of autoantibodies of autoantibody-specific suppressor cells elicited by RBC from various strains of rats.实验性红细胞自身免疫。不同品系大鼠红细胞引发的自身抗体特异性抑制细胞的自身抗体特异性。
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Experimental erythrocyte autoimmunity. I. Mice congenic for immunoglobulin allotypes vary in production of autoantibodies but produce suppressor cells not restricted by allotypes.实验性红细胞自身免疫。I. 免疫球蛋白同种异型基因纯合的小鼠产生自身抗体的情况不同,但能产生不受同种异型限制的抑制细胞。
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Suppression of autoantibodies is specific for the foreign antigens inducing the autoimmunity.自身抗体的抑制作用对诱导自身免疫的外来抗原具有特异性。
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Autoantibody-specific suppressor cells are elicited by membrane components of rat RBC independently of circulating autoantibodies but TNP-specific suppressors are not elicited by TNP-rat RBC.大鼠红细胞的膜成分可诱导自身抗体特异性抑制细胞,这一过程独立于循环自身抗体,但三硝基苯(TNP)特异性抑制细胞不能由TNP修饰的大鼠红细胞诱导产生。
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Expression and regulation of erythrocyte auto-antibodies in mice following immunization with rat erythrocytes.用大鼠红细胞免疫小鼠后红细胞自身抗体的表达与调控
Eur J Immunol. 1989 May;19(5):795-801. doi: 10.1002/eji.1830190503.

引用本文的文献

1
Cyclosporin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in immunoregulatory disorders.环孢素。对其药效学和药代动力学特性以及在免疫调节紊乱中的治疗应用的综述。
Drugs. 1993 Jun;45(6):953-1040. doi: 10.2165/00003495-199345060-00007.
2
Cyclosporine: immunology, toxicity and pharmacology in experimental animals.环孢素:实验动物的免疫学、毒性和药理学
Agents Actions. 1984 Oct;15(3-4):306-27. doi: 10.1007/BF01972366.
3
Cyclosporin A induces long-term unresponsiveness in mercuric chloride-induced autoimmune glomerulonephritis.
环孢素A可诱导氯化汞所致自身免疫性肾小球肾炎的长期无反应性。
Clin Exp Immunol. 1988 Aug;73(2):307-11.
4
In vitro effect of cyclosporin A on immunoglobulin production and concanavalin A induced suppression in primary biliary cirrhosis.环孢素A对原发性胆汁性肝硬化中免疫球蛋白产生及伴刀豆球蛋白A诱导抑制的体外作用
Gut. 1986 Mar;27(3):317-23. doi: 10.1136/gut.27.3.317.