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接触敏感性的非特异性调节机制:非特异性抑制因子(NSF)活性对中间细胞的需求。

Non-specific regulatory mechanism of contact sensitivity: the requirement of intermediate cells for non-specific suppressor factor (NSF) activity.

作者信息

Nakano Y

机构信息

Department of Industrial Health, Osaka Prefectural Institute of Public Health, Japan.

出版信息

Immunology. 1988 Jun;64(2):261-6.

Abstract

Non-specific suppressor factor (NSF), which inhibits passive transfer of contact sensitivity (CS), is produced spontaneously from macrophage-like suppressor cells which were induced by intravenous (i.v.) administration of oxazolone (Ox)-conjugated spleen cells. NSF is absorbed with normal spleen cells, and NSF-treated spleen cells acquire the ability to suppress the transfer of the effector cell function of CS non-specifically. In the present study, the events involved in the suppression by NSF were investigated. The involvement of intermediate cells between NSF and effector T cells in the suppression by NSF was suggested by the following observations: (i) NSF was absorbed with plastic-adherent and cyclophosphamide (CY)-sensitive non-T cells present in normal spleen cells; (ii) deletion of plastic adherent and CY-sensitive cells but not of adult thymectomy (ATx)-sensitive cells from the effector cell population, rendered the effector cells resistant to the suppressor activity of NSF; (iii) reconstitution of CY-pretreated effector cell population with Thy-1-negative spleen cells restored the ability of NSF to suppress CY-pretreated effector cells function. On the contrary, reconstitution with Ia-negative spleen cells did not restore the ability of NSF to suppress CY-pretreated effector cells function. Thus, NSF may not suppress directly the effector T-cell function, but intermediate cells, which are possibly macrophage-like cells, may exert a suppressive role after absorbing NSF. Species specificity was observed between the interaction of NSF and intermediate cells. The possible role of the intermediate cells in the suppression circuit of CS by NSF is discussed.

摘要

非特异性抑制因子(NSF)可抑制接触敏感性(CS)的被动转移,它由静脉注射(i.v.)恶唑酮(Ox)偶联的脾细胞诱导产生的巨噬细胞样抑制细胞自发产生。NSF可被正常脾细胞吸收,经NSF处理的脾细胞获得了非特异性抑制CS效应细胞功能转移的能力。在本研究中,对NSF介导的抑制作用所涉及的事件进行了研究。以下观察结果提示了NSF与效应T细胞之间的中间细胞在NSF介导的抑制作用中的参与:(i)NSF可被正常脾细胞中存在的塑料贴壁且对环磷酰胺(CY)敏感的非T细胞吸收;(ii)从效应细胞群体中去除塑料贴壁且对CY敏感的细胞而非对成年胸腺切除(ATx)敏感的细胞,可使效应细胞对NSF的抑制活性产生抗性;(iii)用Thy-1阴性脾细胞重建经CY预处理的效应细胞群体,可恢复NSF抑制经CY预处理的效应细胞功能的能力。相反,用Ia阴性脾细胞重建则不能恢复NSF抑制经CY预处理的效应细胞功能的能力。因此,NSF可能不会直接抑制效应T细胞的功能,而是中间细胞(可能是巨噬细胞样细胞)在吸收NSF后可能发挥抑制作用。在NSF与中间细胞的相互作用中观察到了物种特异性。讨论了中间细胞在NSF介导的CS抑制回路中的可能作用。

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