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金黄色葡萄球菌诱导的小鼠接触敏感性抑制:多克隆B细胞活化引发的抑制细胞受独特型-抗独特型相互作用调控。

Staphylococcus aureus-induced suppression of contact sensitivity in mice: suppressor cells elicited by polyclonal B-cell activation are regulated by idiotype--anti-idiotype interactions.

作者信息

Benedettini G, De Libero G, Mori L, Marelli P, Angioni M R, Campa M

出版信息

Cell Immunol. 1985 Jul;93(2):508-19. doi: 10.1016/0008-8749(85)90155-8.

Abstract

Staphylococcus aureus strain Cowan I, a strong polyclonal B-cell activator (PBA), inhibited contact sensitivity to oxazolone in mice when administered 24 hr before sensitization. This suppression was mediated by idiotype-positive (Id+) B lymphocytes, which arose very early during the sensitization process and induced anti-Id B cells. These cells were found at Day 3 of the sensitization process and exerted their effect by activating antigen-specific suppressor T lymphocytes, which affected the efferent phase of the immune response. S. aureus strain Wood 46, which lacks of the ability to act as a PBA, was unable to inhibit contact sensitivity. These results indicate that PBA may play an important role in the regulation of cell-mediated immune reactions.

摘要

金黄色葡萄球菌考恩I株是一种强大的多克隆B细胞激活剂(PBA),在致敏前24小时给药时,可抑制小鼠对恶唑酮的接触敏感性。这种抑制作用由独特型阳性(Id+)B淋巴细胞介导,这些细胞在致敏过程中很早就出现,并诱导产生抗Id B细胞。这些细胞在致敏过程的第3天被发现,并通过激活抗原特异性抑制性T淋巴细胞发挥作用,后者影响免疫反应的传出阶段。缺乏作为PBA能力的金黄色葡萄球菌伍德46株无法抑制接触敏感性。这些结果表明,PBA可能在细胞介导的免疫反应调节中起重要作用。

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