Griffiths Kristin L, Tan Jonathan K H, O'Neill Helen C
Research School of Biology, The Australian National University, Canberra, ACT, Australia.
J Cell Mol Med. 2014 Sep;18(9):1908-12. doi: 10.1111/jcmm.12332. Epub 2014 Jun 10.
The Gram-negative bacterial endotoxin lipopolysaccharide (LPS) is a potent inflammatory mediator and a leading cause of bacterial sepsis. While LPS is known to activate antigen-presenting cells, here we find that LPS down-regulates expression of CD11c and CD11b on splenic dendritic cell subsets, thus confounding the ability to identify these subsets following treatment. This has implications with regard to tracking the response to LPS in terms of the cell subsets involved, and should be considered whenever such studies are undertaken.
革兰氏阴性菌内毒素脂多糖(LPS)是一种强效炎症介质,也是细菌性败血症的主要病因。虽然已知LPS可激活抗原呈递细胞,但我们在此发现,LPS会下调脾脏树突状细胞亚群上CD11c和CD11b的表达,从而干扰了处理后对这些亚群的识别能力。这对于追踪涉及的细胞亚群对LPS的反应具有影响,并且在进行此类研究时都应予以考虑。