Noguera Hernando E, Kreisler M, Durantez A, Larrea Gayarre A, de Landazuri M O, Cruz Martínez J
Allergol Immunopathol (Madr). 1978 May-Jun;6(3):253-62.
A number of authors have pointed out a diminution of ADCC (Antibody dependent cellular cytotoxicity) in lymphocytes from peripheral blood of patients with rheumatoid arthritis (RA). It has also been found that the addition of rheumatoid serum inhibits ADCC and also spontaneous cellular cytotoxicity (SCC). This effect could be the result of blocking of effector cell receptors for the Fc fragment of IgG by anti-immunoglobulins and/or immune complexes, present in great quantities in rheumatoid serum. We investigated the effect of synovial fluid on the ADCC and SCC shown by purified suspensions of lymphocytes from healthy donors and RA patients towards chicken erythrocytes tagged with 51 Cr. The samples of synovial fluid from patients with RA or arthrosis did not influence per se the spontaneous release of 51 Cr, once their complement had been removed. Seven-eight of the rheumatoid synovial fluid (RSF) produced a significant decline (p less than 0.01) of SCC. Lymphocytes from the peripheral blood of RA patients showed a greater decline in SCC after the addition of RSF than those from healthy subjects (p less than 0.02). In 14/16 RSF and 5/7 samples of arthrosis synovial fluid (ASF) the ability to diminish ADCC significantly (P less than 0.01) was shown. RSF maintained this inhibitory effect in 1:40 and 1:80 dilutions, whereas in these conditions ASF had no effect on ADCC. RSF and ASF, before their complement was removed, showed an opposite effect, provoking an increase in cytotoxic activity, both SCC and ADCC, though in different proportions. These experiments show that RSF, like rheumatoid serum, inhibits ADCC and SCC, possibly by the same mechanism which blocks the Fc receptors by means of immune complexes, and coincides in its general lines with the recent findings of Díaz Jouanen et al. The pathogenetic implications of this phenomenon are difficult to clarify at present. Its occurrence in vivo would represent the establishment of a local block of cytotoxic effector cells (protector effect), which, on the other hand, would no longer be able to exercise their destructive action against cells responsible for the initiation and/or maintenance of articular damage (pathogenic effect). The non-participation of T cells, in these types of cytotoxicity, previously shown by other authors, accentuates the importance of thymus-independent regulatory systems in the mechanisms which maintain articular damage in RA.
许多作者指出，类风湿性关节炎（RA）患者外周血淋巴细胞中的抗体依赖性细胞毒性（ADCC）有所减弱。还发现，添加类风湿血清会抑制ADCC以及自发细胞毒性（SCC）。这种效应可能是由于类风湿血清中大量存在的抗免疫球蛋白和/或免疫复合物阻断了效应细胞上针对IgG Fc片段的受体。我们研究了滑液对健康供体和RA患者纯化淋巴细胞悬液针对用51 Cr标记的鸡红细胞所表现出的ADCC和SCC的影响。类风湿性关节炎或关节病患者的滑液样本，一旦去除其补体，本身并不会影响51 Cr的自发释放。七分之八的类风湿滑液（RSF）使SCC显著下降（p小于0.01）。添加RSF后，RA患者外周血淋巴细胞的SCC下降幅度比健康受试者的更大（p小于0.02）。在14/16的RSF和5/7的关节病滑液（ASF）样本中，显示出显著降低ADCC的能力（P小于0.01）。RSF在1:40和1:80稀释度下仍保持这种抑制作用，而在这些条件下ASF对ADCC没有影响。RSF和ASF在去除补体之前表现出相反的效果，即引发细胞毒性活性增加，包括SCC和ADCC，尽管比例不同。这些实验表明，RSF与类风湿血清一样，可能通过免疫复合物阻断Fc受体的相同机制来抑制ADCC和SCC，并且在总体上与迪亚兹·乔阿南等人最近的发现一致。目前很难阐明这一现象的发病机制。它在体内的出现将代表细胞毒性效应细胞的局部阻断的建立（保护作用），而另一方面，这些效应细胞将不再能够对引发和/或维持关节损伤的细胞发挥其破坏作用（致病作用）。其他作者先前已表明，T细胞不参与这些类型的细胞毒性，这凸显了非胸腺依赖性调节系统在维持RA关节损伤机制中的重要性。
