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对可溶性肿瘤抗原致敏后肿瘤生长的特异性增强及细胞介导免疫的抑制。

Specific enhancement of tumor growth and depression of cell-mediated immunity following sensitization to soluble tumor antigens.

作者信息

Rao V S, Bonavida B

出版信息

Cancer Res. 1976 Apr;36(4):1384-91.

PMID:56998
Abstract

W/Fu rats inoculated s.c. with less than or equal to 5 x 10(7) syngeneic (C58NT)D (Gross virus-positive) lymphoma tumor cells normally develop a palpable tumor which reaches its maximum size (12 to 14 mm) at 6 to 8 days and is subsequently rejected by 10 to 12 days. However, rats previously sensitized with soluble tumor antigens from (C58NT)D cells prior to (C58NT)D tumor inoculation demonstrate a significant enhancement of tumor growth (the tumor reaches up to 26 mm and is rejected by 16 to 18 days). This enhancement persisted in antigen-treated rats that continued to receive soluble antigen after tumor inoculation. The in vivo enhancement coincided with a significant in vitro depression of cell-mediated cytotoxicity [assessed with 51Cr-labeled (C58NT)D target cells and peripheral blood leukocytes]. The observed tumor enhancement was specific, inasmuch as presensitization to either soluble tumor antigens from WR6 (Gross virus-negative) tumor, syngeneic to W/Fu rats, or to soluble antigen from W/Fu spleen cells had no enhancing effect on (C58NT)D tumor growth. Interestingly, sensitization to soluble tumor antigen alone did not elicit detectable cell-mediated immunity, cytotoxic antibody, or serum-blocking activity to the (C58NT)D tumor. We conclude that sensitization to soluble tumor antigens specifically impairs the immune apparatus normally acting in tumor rejection. This impairment appears to act primarily at the induction phase of the immune response.

摘要

皮下接种小于或等于5×10⁷同基因(C58NT)D(格罗斯病毒阳性)淋巴瘤肿瘤细胞的W/Fu大鼠通常会形成可触及的肿瘤,该肿瘤在6至8天达到最大尺寸(12至14毫米),随后在10至12天被排斥。然而,在接种(C58NT)D肿瘤之前先用(C58NT)D细胞的可溶性肿瘤抗原致敏的大鼠,其肿瘤生长显著增强(肿瘤可达26毫米,并在16至18天被排斥)。这种增强作用在肿瘤接种后继续接受可溶性抗原的抗原处理大鼠中持续存在。体内增强作用与细胞介导的细胞毒性在体外的显著降低相吻合[用⁵¹Cr标记的(C58NT)D靶细胞和外周血白细胞进行评估]。观察到的肿瘤增强是特异性的,因为预先致敏于与W/Fu大鼠同基因的WR6(格罗斯病毒阴性)肿瘤的可溶性肿瘤抗原,或W/Fu脾细胞的可溶性抗原,对(C58NT)D肿瘤生长没有增强作用。有趣的是,单独致敏于可溶性肿瘤抗原不会引发对(C58NT)D肿瘤可检测到的细胞介导免疫、细胞毒性抗体或血清阻断活性。我们得出结论,对可溶性肿瘤抗原的致敏特异性损害了正常参与肿瘤排斥的免疫机制。这种损害似乎主要作用于免疫反应的诱导阶段。

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