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[环磷酰胺诱导的伤寒沙门菌VI抗原耐受性的机制]

[Mechanism of tolerance to VI-antigen of Salmonella typhi induced by cyclophosphane].

作者信息

Prigozhina T B, Fontalin L N

出版信息

Biull Eksp Biol Med. 1977 Apr;83(4):440-3.

PMID:558024
Abstract

High dose Vi-antigen treatment and injection of cyclophosphamide 46 to 48 hours later induced in mice a state of immunological unresponsiveness remaining stable in adoptive transfer. Only low amounts of the antigen were revealed in the blood and spleen of tolerant animals 2 to 3 weeks after the tolerogenic treatment. No T-suppressors were found in the spleen of tolerant mice--the cells of tolerant mice failed to suppress the immune response of normal lymphocytes when transferred together to the irradiated recipients, or to induce tolerance in normal mice. Normal spleen cells restored partially the immune responsiveness in tolerant animals. The results obtained suggest that cyclophosphamide tolerance was due to deletion or the long-term inactivation of the immunocompetent cells.

摘要

高剂量Vi抗原处理并在46至48小时后注射环磷酰胺,可在小鼠中诱导出一种免疫无反应状态,这种状态在过继转移中保持稳定。在致耐受性处理后2至3周,仅在耐受动物的血液和脾脏中检测到少量抗原。在耐受小鼠的脾脏中未发现T抑制细胞——耐受小鼠的细胞与正常淋巴细胞一起转移至受辐照受体时,无法抑制正常淋巴细胞的免疫反应,也无法在正常小鼠中诱导耐受性。正常脾细胞可部分恢复耐受动物的免疫反应性。所得结果表明,环磷酰胺诱导的耐受性是由于免疫活性细胞的缺失或长期失活所致。

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