FUNCTIONAL INACTIVATION OF SUPPRESSOR T CELLS BY HEAT-KILLED MACROPHAGES
FUNCTIONAL INACTIVATION OF SUPPRESSOR T CELLS BY HEAT-KILLED MACROPHAGES
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DOI：
10.1038/262216a0
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发表时间：
1976-01-01
期刊：
影响因子：
64.8
通讯作者：
PTAK, W
中科院分区：
文献类型：
--
作者：
GERSHON, RK;EARDLEY, DD;PTAK, W
我们已经证明，在56°C加热30min杀死腹膜渗出巨噬细胞，可以显著抑制原代michell - dutton培养中对异种红细胞的抗体反应1。在嗜细胞抗体存在的情况下，这种热处理不会破坏巨噬细胞与羊红细胞（srbc）形成玫瑰花结的能力，这表明一些膜表面没有受到损害。然而，热处理确实阻止巨噬细胞排除台盼蓝染料，这表明细胞不再存活。在较高温度下或用0.1%戊二醛处理巨噬细胞，会破坏巨噬细胞形成玫瑰花的能力，并抑制mishell - dutton培养。通过蔗糖梯度分离纯化的巨噬细胞膜可以起到类似的作用，即在嗜细胞抗体存在的情况下，抑制原代michell - dutton培养并与srbc形成玫瑰花结。热杀伤巨噬细胞不降低细胞培养的生存能力，即使他们是最大限度的抑制。我们对这些结果的解释表明，死亡的巨噬细胞通过吸收掉一些细胞相互作用所必需的因素，从而抑制了培养中的免疫反应，这些因素导致斑块形成细胞的产生。热杀伤巨噬细胞吸收混合淋巴细胞反应上清液中辅助活性的能力支持了这一论点（W.P.和r.k.g.，未发表）。我们推断，如果巨噬细胞能够吸收相互作用因子，那么如果将巨噬细胞添加到发生抑制的培养物中，它们可能也能够吸收抑制因子，从而增强抑制而非正常培养物的反应。
WE have Shown that peritoneal exudate macrophages, killed by heating at 56 °C for 30min, can markedly suppress the antibody response to heterologous erythrocytes in primary Mishell–Dutton cultures1. This heat treatment does not destroy the ability of the macrophages to form rosettes with sheep red blood cells (SRBCs) in the presence of cytophilic antibody, suggesting that some membrane surfaces remain undamaged. The heat treatment, however, does prevent the macrophages from excluding Trypan blue dye, indicating that the cells are no longer viable. Treatment of the macrophages at higher temperatures or with 0.1% glutaraldehyde destroys both their ability to form rosettes and to suppress Mislhell–Dutton cultures. Macrophage membranes, semppurified by separation on sucrose gradients, can act similarly—that is, suppress primary Mishell–Dutton cultures and form rosettes with SRBCs in the presence of cytophilic antibody (W.P. and R.K.G., unpublished). The heat-killed macrophages do not diminish the viability of the cell cultures even when they are maximally suppressive. We have interpreted these results to indicate that the dead macrophages suppress the immune response in culture by absorbing out, and thus rendering inoperative, some factors which are necessary for the cell interactions which result in the generation of plaque-forming cells. This contention is supported by the ability of the heat-killed macrophages to absorb out the helper activity found in the supernatants of mixed lymphocyte reactions (W.P. and R.K.G., unpublished). We reasoned that, if macrophages could absorb interaction factors, they might be able to absorb suppressive factors if they were added to a culture in which suppression was occurring and thus augment the response of suppressed but not normal cultures.