Coleman J W
Department of Pharmacology and Therapeutics, University of Liverpool, U.K.
Immunology. 1990 Jan;69(1):150-4.
Conditioned medium (CM) from concanavalin A (Con A)-stimulated murine spleen cells inhibited release of histamine and 5-HT from murine peritoneal mast cells sensitized with monoclonal IgE anti-DNP antibody and challenged with DNP-human serum albumin (HSA) antigen. Inhibition was seen when the CM was added to the mast cells either 24 hr before or simultaneous with, but not 24 hr subsequent to, the IgE, thus showing that inhibition was at the IgE-dependent stage of mast cell sensitization. Unconditioned medium, prepared in the same way as CM but not exposed to spleen cells was without activity, demonstrating that inhibition was due to a spleen cell-derived factor. CM from unstimulated spleen cells was likewise without activity. The sensitization inhibitory factor appears to be a protein, since it was retained upon dialysis, and destroyed by heating at 70 degrees and above. The factor does not appear to be IgE, since it was stable at 56 degrees, and is not IL-1 or IL-2, since recombinant human IL-1 alpha and IL-1 beta, and recombinant mouse IL-1 alpha and IL-2 were without inhibitory activity. The active CM and all recombinant IL-1 and IL-2 preparations did not release histamine or 5-HT directly from mast cells during 48 hr of culture, and did not modulate the histamine content of these cells, nor their capacity to incorporate [3H]5-HT.
来自伴刀豆球蛋白A（Con A）刺激的小鼠脾细胞的条件培养基（CM）抑制了用单克隆IgE抗DNP抗体致敏并用DNP-人血清白蛋白（HSA）抗原攻击的小鼠腹膜肥大细胞中组胺和5-羟色胺的释放。当在IgE加入前24小时或与IgE同时加入CM到肥大细胞时可观察到抑制作用，但在IgE加入后24小时加入则无抑制作用，这表明抑制作用发生在肥大细胞致敏的IgE依赖阶段。以与CM相同的方式制备但未接触脾细胞的未条件培养基没有活性，这表明抑制作用是由于一种脾细胞衍生因子所致。来自未刺激脾细胞的CM同样没有活性。致敏抑制因子似乎是一种蛋白质，因为它在透析后仍保留，并且在70度及以上加热时被破坏。该因子似乎不是IgE，因为它在56度时稳定，并且不是IL-1或IL-2，因为重组人IL-1α和IL-1β以及重组小鼠IL-1α和IL-2均无抑制活性。活性CM和所有重组IL-1和IL-2制剂在48小时培养期间均未直接从肥大细胞释放组胺或5-羟色胺，也未调节这些细胞的组胺含量及其摄取[3H]5-羟色胺的能力。
