Fahmi H, Chaby R
Equipe Endotoxines, URA-1116 du Centre National de la Recherche Scientifique, Université de Paris-Sud, Orsay, France.
J Leukoc Biol. 1993 Jan;53(1):45-52. doi: 10.1002/jlb.53.1.45.
Tolerance of macrophages to endotoxin (lipopolysaccharide, LPS) can be induced in vitro by LPS itself. We show here that one of the mechanisms of tolerance to LPS can be mediated via an autocrine process. Continuous exposure to LPS is not required to induce macrophage desensitization. Refractoriness to production of tumor necrosis factor (TNF) in response to LPS can be transferred from tolerant to naive macrophage populations by incubation of the latter with the culture supernatant of the former, in the absence of endotoxin. The active factor present in this macrophage-desensitizing culture supernatant (MD-Sup) is more efficiently removed by incubation with tolerant macrophages than by incubation with naive macrophages. The refractoriness elicited by treatment with MD-Sup is restricted to a decreased TNF response to LPS; interleukin-1 (IL-1) and IL-6 responses are not affected.
巨噬细胞对内毒素（脂多糖，LPS）的耐受性可在体外由LPS自身诱导产生。我们在此表明，LPS耐受性的机制之一可通过自分泌过程介导。诱导巨噬细胞脱敏并不需要持续暴露于LPS。在无内毒素的情况下，将未致敏巨噬细胞群体与耐受巨噬细胞群体的培养上清共同孵育，可使前者对LPS产生肿瘤坏死因子（TNF）的反应性降低，并将这种耐受性传递给未致敏巨噬细胞群体。与未致敏巨噬细胞孵育相比，与耐受巨噬细胞孵育能更有效地去除这种巨噬细胞脱敏培养上清（MD-Sup）中存在的活性因子。用MD-Sup处理引发的反应性降低仅限于对LPS的TNF反应减弱；白细胞介素-1（IL-1）和IL-6反应不受影响。
