Guéry J C, Tournade H, Pelletier L, Druet E, Druet P
Unité 28, Institut National de la Santé et de la Recherche Médicale, Hôpital Broussais, Paris, France.
Eur J Immunol. 1990 Jan;20(1):101-5. doi: 10.1002/eji.1830200115.
Cross-reactive idiotypes (CRId) borne on autoanti-glomerular basement membrane antibodies of Brown-Norway (BN) rats with mercury-induced glomerulonephritis have been described in the preceding study (Guéry, J.-C. et al., Eur. J. Immunol. 1990. 20:93). BN rats treated with sodium aurothiopropanol sulfonate or D-penicillamine, as well as (LEW X BN)F1 hybrids transferred with BN rat spleen cells, developed quite similar autoimmune abnormalities. In the present study, it is shown that immunoglobulins bearing such "public" idiotypes are also produced and deposited in the kidney in these three models. The CRId here described may, therefore, be considered as a marker of sets of recurrently expressed V region genes during the course of these autoimmune disorders. Anti-self class II T cells are present in the three models of toxin-induced autoimmunity and anti-allo class II T cells are responsible for the chronic graft-vs.-host reaction. The same B cell clones are probably triggered during these processes as a consequence of a polyclonal B cell activation mediated by anti-class II T cells.
在前一项研究中(Guéry, J.-C.等人,《欧洲免疫学杂志》,1990年,20:93),已描述了患有汞诱导性肾小球肾炎的Brown-Norway(BN)大鼠的自身抗肾小球基底膜抗体所携带的交叉反应性独特型(CRId)。用金硫代丙醇磺酸钠或D-青霉胺处理的BN大鼠,以及转输了BN大鼠脾细胞的(LEW×BN)F1杂种鼠,都出现了非常相似的自身免疫异常。在本研究中,结果表明在这三种模型中,携带此类“公共”独特型的免疫球蛋白也在肾脏中产生并沉积。因此,这里所描述的CRId可被视为这些自身免疫性疾病过程中反复表达的V区基因集的一个标志物。抗自身II类T细胞存在于毒素诱导的自身免疫的三种模型中,而抗同种异体II类T细胞则导致慢性移植物抗宿主反应。由于抗II类T细胞介导的多克隆B细胞活化,在这些过程中可能触发了相同的B细胞克隆。