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CD4+抑制细胞数量减少,随后CD8+保护性T细胞扩增,以此解释T细胞缺陷的BALB/c小鼠对利什曼原虫抵抗力增强这一矛盾状态。

Reduced numbers of CD4+ suppressor cells with subsequent expansion of CD8+ protective T cells as an explanation for the paradoxical state of enhanced resistance to Leishmania in T-cell deficient BALB/c mice.

作者信息

Hill J O

机构信息

Trudeau Institute Inc., Saranac Lake, New York 12983.

出版信息

Immunology. 1991 Feb;72(2):282-6.

Abstract

Compared to their normal, T-cell competent counterparts, BALB/c mice that have been thymectomized, lethally irradiated, and reconstituted with bone marrow cells (TXB) were found to be resistant to Leishmania major. Even though TXB mice possess less than 30% of the normal number of T cells in their lymphoid organs, they generated a protective immune response that prevented the progressive multiplication of the parasite in the primary cutaneous lesion and its dissemination to distant visceral sites. Studies of TXB mice depleted of residual CD4+ or CD8+ T cells by systemic monoclonal antibody (mAb) treatment showed that this protective immunity depends on a residual, radio-resistant CD8+ T-cell population, and that it develops in the virtual absence of CD4+ T cells. This immune response can be negated by an infusion of CD4+ T cells from normal susceptible donors, provided that the donor cells are infused before the recipients' response is generated. It is therefore apparant that TXB BALB/c mice are more resistant than T-cell competent BALB/c mice because the former mice lack a threshold number of CD4+ suppressor T cells necessary to down-regulate the induction and expansion of CD8+ protective T cells.

摘要

与正常的具有T细胞功能的同系物相比,已接受胸腺切除、致死性照射并用骨髓细胞重建的BALB/c小鼠(TXB小鼠)被发现对硕大利什曼原虫具有抗性。尽管TXB小鼠淋巴器官中的T细胞数量不到正常数量的30%,但它们产生了一种保护性免疫反应,阻止了寄生虫在原发性皮肤病变中进行性增殖并扩散到远处的内脏部位。通过全身单克隆抗体(mAb)处理耗尽残余CD4+或CD8+ T细胞的TXB小鼠研究表明,这种保护性免疫依赖于残余的、对辐射有抗性的CD8+ T细胞群体,并且它在几乎没有CD4+ T细胞的情况下发展。如果在受体产生反应之前注入来自正常易感供体的CD4+ T细胞,这种免疫反应可以被消除。因此,很明显TXB BALB/c小鼠比具有T细胞功能的BALB/c小鼠更具抗性,因为前者小鼠缺乏下调CD8+保护性T细胞诱导和扩增所需的阈值数量的CD4+抑制性T细胞。

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