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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CD6 binds to pathogen-associated molecular patterns and protects from LPS-induced septic shock
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CD6 binds to pathogen-associated molecular patterns and protects from LPS-induced septic shock

机译：CD6结合病原体相关的分子模式，并保护免受LPS诱导的败血性休克

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摘要

CD6 is a lymphocyte receptor that belongs to the scavenger receptor cysteine-rich superfamily. Because some members of the scavenger receptor cysteine-rich superfamily act as pattern recognition receptors for microbial components, we studied whether CD6 shares this function. We produced a recombinant form of the ectodomain of CD6 (rsCD6), which was indistinguishable (in apparent molecular mass, antibody reactivity, and cell binding properties) from a circulating form of CD6 affinity-purified from human serum. rsCD6 bound to and aggregated several Gram-positive and -negative bacterial strains through the recognition of lipoteichoic acid and LPS, respectively. The K_d of the LPS-rsCD6 interaction was 2.69 ± 0.32 x 10~(-8) M, which is similar to that reported for the LPS-CD14 interaction. Further experiments showed that membrane CD6 also retains the LPS-binding ability, and it results in activation of the MAPK signaling cascade. In vivo experiments demonstrated that i.p. administration of rsCD6 before lethal LPS challenge significantly improved mice survival, and this was concomitant with reduced serum levels of the proinflammatory cyto-kines TNF-α, IL6, and IL-1β. In conclusion, our results illustrate the unprecedented bacterial binding properties of rsCD6 and support its therapeutic potential for the intervention of septic shock syndrome or other inflammatory diseases of infectious origin.
机译：CD6是一种淋巴细胞受体，属于清除剂受体富含半胱氨酸的超家族。由于清道夫受体富含半胱氨酸的超家族的某些成员充当微生物成分的模式识别受体，因此我们研究了CD6是否具有此功能。我们生产了CD6胞外域的重组形式（rsCD6），与从人血清中亲和纯化的CD6循环形式没有区别（表观分子量，抗体反应性和细胞结合特性）。 rsCD6分别通过识别脂磷壁酸和LPS结合并聚集了几个革兰氏阳性和阴性细菌菌株。 LPS-rsCD6相互作用的K_d为2.69±0.32 x 10〜（-8）M，与报道的LPS-CD14相互作用的K_d相似。进一步的实验表明，膜CD6还保留了LPS结合能力，并导致MAPK信号级联反应的激活。体内实验表明在致死性LPS攻击前施用rsCD6可以显着提高小鼠存活率，这与血清促炎性细胞因子TNF-α，IL6和IL-1β的水平降低有关。总之，我们的结果表明rsCD6具有空前的细菌结合特性，并支持其治疗败血性休克综合征或其他传染源性炎症性疾病的治疗潜力。

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