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在注射了结核分枝杆菌纯化蛋白衍生物的小鼠中,抑制性T细胞以及抗半抗原和抗独特型B淋巴细胞调节对恶唑酮的接触敏感性。

T suppressor cells as well as anti-hapten and anti-idiotype B lymphocytes regulate contact sensitivity to oxazolone in mice injected with purified protein derivative from Mycobacterium tuberculosis.

作者信息

Campa M, Benedettini G, De Libero G, Mori L, Falcone G

出版信息

Infect Immun. 1984 Sep;45(3):701-7. doi: 10.1128/iai.45.3.701-707.1984.

Abstract

Purified protein derivative from Mycobacterium tuberculosis inhibits contact sensitivity to oxazolone in mice when given intravenously 24 to 72 h before the antigen. Transfer experiments showed that various types of suppressor cells occurred in the lymph nodes draining the site of sensitization: (i) anti-oxazolone idiotype + B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients at the moment of their sensitization; (ii) anti-idiotype B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients when sensitization of these animals had been performed 3 days before cell transfer; (iii) T lymphocytes, found only at day 6 after sensitization, inhibited the passive transfer of contact sensitivity, indicating that they were effective on the efferent phase of the immune response. These results indicate that purified protein derivative from M. tuberculosis interferes with contact sensitivity by activating a complex and multiple immunoregulatory circuit.

摘要

结核分枝杆菌纯化蛋白衍生物在抗原注射前24至72小时静脉注射时,可抑制小鼠对恶唑酮的接触敏感性。转移实验表明,在致敏部位引流的淋巴结中出现了各种类型的抑制细胞:(i)抗恶唑酮独特型+B淋巴细胞,在致敏后第3天发现,在致敏时将抑制作用转移给同基因受体;(ii)抗独特型B淋巴细胞,在致敏后第3天发现,当这些动物在细胞转移前3天进行致敏时,将抑制作用转移给同基因受体;(iii)仅在致敏后第6天发现的T淋巴细胞,抑制接触敏感性的被动转移,表明它们在免疫反应的传出阶段起作用。这些结果表明,结核分枝杆菌纯化蛋白衍生物通过激活一个复杂的多重免疫调节回路来干扰接触敏感性。

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本文引用的文献

4
Staphylococcus aureus inhibits contact sensitivity to oxazolone by activating suppressor B cells in mice.
Int Arch Allergy Appl Immunol. 1984;73(3):269-73. doi: 10.1159/000233480.
9
Active pulmonary tuberculosis with negative tuberculin skin reactions.
Am Rev Respir Dis. 1967 Mar;95(3):411-8. doi: 10.1164/arrd.1967.95.3.411.

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