Shimizu S, Sugai S, Imaoka T, Sawada M, Konda S
Scand J Rheumatol Suppl. 1986;61:106-10.
Monoclonal anti-idiotypic antibodies (mA-IDs) were produced against IgM-K, IgA-L and IgA-K monoclonal rheumatoid factors (mRFs), respectively, derived from patients with Sjögren's syndrome (SS). Each mA-ID inhibited the RF activity of the autologous M-protein, but did not inhibit the activity of the other mRFs. As for the specificity of mA-IDs, it was confirmed to bind only to the mRF used for immunization. A cross-reactive idiotype (CRI) was detected in 3 out of 106 polyclonal RFs (pRFs) using AW5/3 mA-ID by double immunodiffusion or ELISA inhibition assay on pRF activity. However, no CRI was detected on AMB1/5 or SF18/2 mA-ID. One of the mA-IDs, AW5/3, cross-reacted with nuclei of proliferating lymphocytes, such as PHA-stimulated lymphocytes, interleukin 2 dependent T cell lines, B-lymphoblastoid cell lines or cultured lymphoma cell lines, but barely reacted with nuclei of normal resting lymphocytes.
分别针对来自干燥综合征(SS)患者的IgM-K、IgA-L和IgA-K单克隆类风湿因子(mRFs)制备了单克隆抗独特型抗体(mA-IDs)。每种mA-ID均抑制自身M蛋白的RF活性,但不抑制其他mRFs的活性。至于mA-IDs的特异性,已证实其仅与用于免疫的mRF结合。通过对多克隆RFs(pRFs)进行双免疫扩散或ELISA抑制试验,使用AW5/3 mA-ID在106个pRFs中的3个中检测到交叉反应独特型(CRI)。然而,在AMB1/5或SF18/2 mA-ID上未检测到CRI。其中一种mA-ID,AW5/3,与增殖淋巴细胞的细胞核发生交叉反应,如PHA刺激的淋巴细胞、白细胞介素2依赖性T细胞系、B淋巴母细胞系或培养的淋巴瘤细胞系,但与正常静息淋巴细胞的细胞核几乎不发生反应。