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肿瘤免疫中的差异性抗原呈递。

Differential antigen presentation in tumor immunity.

作者信息

Schatten S, Drebin J A, Granstein R D, Greene M I

出版信息

Fed Proc. 1984 Jun;43(9):2460-4.

PMID:6327399
Abstract

The tumor S1509a elicits a cell-mediated immune response in immune A/J mice but leads to the generation of suppressor T cells (Ts) in nonimmune mice. Previous studies have shown that I-A+ antigen-presenting cells (APC) present S1509a tumor antigen and thereby activate immune T cells. Recent studies with polyoma-induced tumors reveal similar findings. Administration of anti-I-A antibodies not only prevents effective T cell activation by I-A+ APC bearing S1509a tumor antigen but also induces Ts after a tumor challenge. Ts, which inhibit S1509a tumor immunity, may be activated by tumor antigen presented on I-J+ APC. Examination of the immunologic effects of cyclophosphamide and UV radiation supports this hypothesis.

摘要

肿瘤S1509a在免疫A/J小鼠中引发细胞介导的免疫反应,但在非免疫小鼠中导致抑制性T细胞(Ts)的产生。先前的研究表明,I-A+抗原呈递细胞(APC)呈递S1509a肿瘤抗原,从而激活免疫T细胞。最近关于多瘤病毒诱导肿瘤的研究也有类似发现。给予抗I-A抗体不仅会阻止携带S1509a肿瘤抗原的I-A+ APC有效激活T细胞,还会在肿瘤攻击后诱导Ts。抑制S1509a肿瘤免疫的Ts可能由I-J+ APC呈递的肿瘤抗原激活。对环磷酰胺和紫外线辐射免疫效应的研究支持了这一假设。

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