Ginsburg C H, Wisniewski E, Greene M I
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Immunology. 1987 Nov;62(3):335-40.
Antibody regulation of hapten-specific granulomas was studied in mice in order to assess the relationship between an anti-idiotypic antibody and granuloma formation. An anti-idiotypic antibody was raised against the idiotype of an azobenzenearsonate (ABA)-specific antibody of A/J mice. The anti-idiotypic antibody was subcutaneously (s.c.) administered to syngeneic mice prior to challenge with ABA-coupled polyacrylamide beads injected into the intestinal wall. The results of such a challenge were assessed histologically for granuloma formation at 24-h intervals. Mice primed with anti-Id antibody and challenged with ABA-linked beads developed epithelioid granulomas at 72 and 96 hr post-challenge. Unprimed mice or mice primed with control antibodies did not develop granulomas when challenged with ABA-linked beads. Moreover, we found that priming with anti-Id antibody intravenously (i.v.) resulted in suppression of intestinal granuloma formation that was similar to that observed previously after priming mice i.v. with ABA-coupled spleen cells (Ginsburg et al., 1982). This study demonstrates the induction and suppression of hapten-specific granuloma formation in the intestine by an anti-Id antibody. The observations indicate a role for the idiotype-anti-idiotype interaction in regulation of hapten-specific granuloma formation, and may have implications for the manner in which the host reacts against self in the autoimmune inflammatory process.
为了评估抗独特型抗体与肉芽肿形成之间的关系，我们在小鼠中研究了半抗原特异性肉芽肿的抗体调节作用。针对A/J小鼠的偶氮苯砷酸盐（ABA）特异性抗体的独特型产生了一种抗独特型抗体。在用注入肠壁的ABA偶联聚丙烯酰胺珠进行攻击之前，将抗独特型抗体皮下注射给同基因小鼠。每隔24小时对这种攻击的结果进行组织学评估以观察肉芽肿形成情况。用抗Id抗体致敏并用ABA连接的珠子攻击的小鼠在攻击后72小时和96小时出现上皮样肉芽肿。未致敏的小鼠或用对照抗体致敏的小鼠在用ABA连接的珠子攻击时未形成肉芽肿。此外，我们发现静脉注射抗Id抗体致敏会导致肠道肉芽肿形成受到抑制，这与之前静脉注射ABA偶联脾细胞致敏小鼠后观察到的情况相似（金斯伯格等人，1982年）。这项研究证明了抗Id抗体在肠道中对半抗原特异性肉芽肿形成的诱导和抑制作用。这些观察结果表明独特型-抗独特型相互作用在半抗原特异性肉芽肿形成的调节中起作用，并且可能对宿主在自身免疫炎症过程中对自身的反应方式有影响。
