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首页> 外文期刊>Cellular immunology >Chondrocyte-specific phenotype confers susceptibility of rat chondrocytes to lysis by NK cells.
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Chondrocyte-specific phenotype confers susceptibility of rat chondrocytes to lysis by NK cells.

机译：软骨细胞特异性表型赋予大鼠软骨细胞以NK细胞溶解的敏感性。

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摘要

Normal chondrocytes are targets for natural killer (NK) cells. Since the mechanism of this phenomenon remains unknown, the present study was aimed at testing whether it is associated with chondrocyte-specific phenotype defined as ability of cartilage cells to produce sulfated glycosaminoglycans (GAG) and express collagen II and aggrecan mRNA. Lysis of rat epiphyseal chondrocytes by syngeneic spleen mononuclear cells (SMCs) was evaluated by (51)Cr-release assay. Loss of chondrocyte phenotype following long-term culture resulted in their decreased susceptibility to lysis. Similar effect was also observed after suppression of chondrocyte phenotype by TNF. On the other hand, stimulation of cartilage-specific matrix component synthesis by IGF-1 resulted in increased chondrocyte killing and exogenous chondroitin sulfate A stimulated NK cell-mediated cytotoxicity against chondrocytes and human K562 cells. This suggests that chondrocyte susceptibility to lysis by NK cells depends on chondrocyte-specific phenotype, especially sulfated GAG production.
机译：正常的软骨细胞是自然杀伤（NK）细胞的目标。由于这种现象的机制仍然未知，因此本研究旨在测试其是否与软骨细胞特异性表型有关，该表型定义为软骨细胞产生硫酸化糖胺聚糖（GAG）并表达胶原蛋白II和聚集蛋白聚糖的能力。用（51）Cr-释放试验评估同基因脾单核细胞（SMCs）对大鼠epi干软骨细胞的裂解作用。长期培养后软骨细胞表型的丧失导致其对溶解的敏感性降低。 TNF抑制软骨细胞表型后，也观察到类似的效果。另一方面，IGF-1刺激软骨特异性基质成分的合成导致软骨细胞杀伤增加和外源硫酸软骨素A刺激了NK细胞介导的针对软骨细胞和人K562细胞的细胞毒性。这表明软骨细胞对NK细胞裂解的敏感性取决于软骨细胞特异性表型，尤其是硫酸化GAG的产生。

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