Negative feedback regulation of contact sensitivity to DNFB by autoanti-idiotypic antibody.
Negative feedback regulation of contact sensitivity to DNFB by autoanti-idiotypic antibody.
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自身抗独特型抗体对 DNFB 接触敏感性的负反馈调节。
DOI：
10.1111/j.1749-6632.1982.tb36120.x
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发表时间：
1982
影响因子：
5.2
通讯作者：
Moorhead,JW
中科院分区：
文献类型：
--
作者：
Moorhead,JW
对2，4-二硝基氟苯的接触敏感性在致敏后6天最高，但由于宿主产生的自身抗独特型抗体而迅速下降。这里提出的研究表明，这种下调抗Id是一个C-独立的主动过程，涉及免疫淋巴结细胞群中的Ia + T细胞的子集。消耗Ia + T细胞的免疫LN细胞使其对单独抗Id的抑制不敏感，尽管抗Id加C的处理抑制了相同的群体。通过加入未处理的DNFB致敏的LN细胞而不是通过加入正常LN细胞，使该细胞群对单独的抗Id抑制敏感。进一步的研究表明，抗Id激活的Ia + T细胞的抑制发生在皮肤试验部位局部，并且是抗原非特异性的。这些数据表明，CS DNFB的自身抗Id抗体的自然调节涉及负反馈调节环。
Contact sensitivity to 2, 4-dinitrofluorobenzene is maximal six days after sensitization but declines rapidly, due to autoanti-idiotypic antibodies produced by the host. The studies presented here indicate that this down regulation by anti-Id is a C-independent active process involving a subset of Ia+ T cells in the immune lymph node cell population. Depleting immune LN cells of Ia+ T cells renders them insensitive to inhibition by anti-Id alone, although the same population is inhibited by treatment anti-Id plus C. This cell population is rendered sensitive to inhibition by anit-Id alone by adding untreated DNFB-sensitized LN cells but not by adding normal LN cells. Further studies showed that suppression by anti-Id-activated Ia+ T cells occurs locally at the skin test site and is antigen nonspecific. These data indicate that the natural regulation of CS to DNFB by autoanti-Id antibodies involves a negative feedback regulatory loop.