Cohen P L, Eisenberg R A
J Exp Med. 1982 Jul 1;156(1):173-80. doi: 10.1084/jem.156.1.173.
The F1 hybrids of NZB and several normal mouse strains are known to produce less anti-erythrocyte (Coombs) autoantibody and develop a milder hemolytic anemia than their NZB parents. We have found that serum from some (NZB x CBA)F1 mice agglutinated erythrocytes from certain Coombs-positive NZB mice, often in extremely high titer, whereas other (CBA x NZB)F1 sera agglutinated erythrocytes from different individual NZB mice. The agglutination was due to antibody, but was not due to rheumatoid factor activity. Because F(ab')2 fragments of the F1 sera agglutinated erythrocytes coated with F(ab')2 fragments of the appropriate NZB sera, the observed reactivity was probably caused by idiotype-anti-idiotype interactions. In addition, because F1 sera could not agglutinate mouse erythrocytes coated with monovalent NZB Fab' fragments, the recognized idiotype probably involved the antigen-binding site. Anti-idiotypic antibodies against anti-erythrocyte autoantibodies may play an important role in the regulation of autoantibody formation.
已知新西兰黑鼠（NZB）与几种正常小鼠品系的F1杂种产生的抗红细胞（库姆斯）自身抗体比其NZB亲本少，且发生的溶血性贫血也较轻。我们发现，一些（NZB×CBA）F1小鼠的血清能凝集某些库姆斯阳性NZB小鼠的红细胞，凝集效价通常极高，而其他（CBA×NZB）F1血清则能凝集不同个体NZB小鼠的红细胞。这种凝集是由抗体引起的，但不是由类风湿因子活性导致的。由于F1血清的F(ab')2片段能凝集包被有相应NZB血清F(ab')2片段的红细胞，所以观察到的反应性可能是由独特型-抗独特型相互作用引起的。此外，由于F1血清不能凝集包被有单价NZB Fab'片段的小鼠红细胞，所以识别的独特型可能涉及抗原结合位点。抗红细胞自身抗体的抗独特型抗体可能在自身抗体形成的调节中起重要作用。
