Mossmann H, Lauer W, Vortisch U, Gunther E, Bazin H, Hammer D K
Eur J Immunol. 1976 Aug;6(8):591-4. doi: 10.1002/eji.1830060813.
The stimulatory as well as the inhibitory capacity of alloantisera has been investigated with respect to rat mast cell functions. Alloantibody against alloantigens coded for by the major histocompatibility (H-1) gene region promoted histamine release from purified LEW mast cells. This process was found to be complement-independent but demonstrated an absolute requirement for calcium. Pretreatment of mast cells with anti-H-1 antisera in the absence of calcium markedly suppressed the IgE-dependent histamine release challenged either by antigen or by anti-IgE antibody. The alloantisera, however, did not interfere with the ability of compound 48/80-associated histamine liberation. Additionally, antibodies specific for H-1 antigens were highly effective in inhibiting the binding of IgE to the mast cell surface. Alloantisera absorbed with erythrocytes lost their capacity to block mast cell functions. Based on these data the possible ralationship between H-1 alloantigens and the IgE receptor on the mast cell surface is discussed.
就大鼠肥大细胞功能而言，已对同种抗血清的刺激能力和抑制能力进行了研究。针对主要组织相容性（H-1）基因区域编码的同种抗原的同种抗体促进了纯化的LEW肥大细胞中组胺的释放。发现该过程不依赖补体，但表明绝对需要钙。在无钙的情况下用抗H-1抗血清预处理肥大细胞，可显著抑制由抗原或抗IgE抗体激发的IgE依赖性组胺释放。然而，同种抗血清并不干扰化合物48/80相关的组胺释放能力。此外，对H-1抗原特异的抗体在抑制IgE与肥大细胞表面结合方面非常有效。用红细胞吸收的同种抗血清失去了阻断肥大细胞功能的能力。基于这些数据，讨论了H-1同种抗原与肥大细胞表面IgE受体之间可能的关系。
