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白色念珠菌在小鼠淋巴瘤模型中的佐剂活性的细胞机制。

Cellular mechanisms underlying the adjuvant activity of Candida albicans in a mouse lymphoma model.

作者信息

Marconi P, Cassone A, Tissi L, Baccarini M, Puccetti P, Garaci E, Bonmassar E, Bistoni F

出版信息

Int J Cancer. 1982 Apr 15;29(4):483-8. doi: 10.1002/ijc.2910290420.

Abstract

Inactivated Candida albicans (CA) possesses strong anti-tumor activity when combined with cytoreductive chemotherapy in a mouse lymphoma model. In the present study, experiments were performed in order to elucidate the mechanism(s) underlying CA immunoadjuvant activity. In vivo chemotherapy studies proved that the synergistic anti-tumor effects were lost in athymic (nu/nu) mice and were also abrogated by radiations. In vitro tests did not suggest a major involvement of natural cytotoxic effectors such as macrophages and natural killer cells nor did CA effects appear to be mediated by induction of interferon. It was concluded that the immunoadjuvant activity of CA largely relies on host responses against tumor-associated transplantation antigens with no major involvement of natural resistance immune mechanisms.

摘要

在小鼠淋巴瘤模型中,灭活白色念珠菌(CA)与减瘤化疗联合使用时具有很强的抗肿瘤活性。在本研究中,进行了实验以阐明CA免疫佐剂活性的潜在机制。体内化疗研究证明,无胸腺(裸鼠)小鼠失去了协同抗肿瘤作用,并且辐射也消除了这种作用。体外试验并未表明巨噬细胞和自然杀伤细胞等天然细胞毒性效应器有主要参与,CA的作用似乎也不是由干扰素诱导介导的。得出的结论是,CA的免疫佐剂活性很大程度上依赖于宿主对肿瘤相关移植抗原的反应,而天然抗性免疫机制没有主要参与。

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