Yang D, Howard O M, Chen Q, Oppenheim J J
Laboratory of Molecular Immunoregulation, Division of Basic Sciences, Science Applications International Corp.-Frederick Cancer Research and Develeopment Center, National Cancer Institute, MD 21702, USA.
J Immunol. 1999 Aug 15;163(4):1737-41.
Although CD34+ progenitor-derived immature dendritic cells (DCs) express CCR6, several recent studies reported that monocyte-derived immature DCs do not do so. We observed that DCs generated from monocytes in the presence of GM-CSF, IL-4, and TGF-beta 1 consistently responded to liver and activation-regulated chemokine (LARC, also known as macrophage inflammatory protein-3 alpha). These immature DCs expressed one class of high-affinity binding sites for LARC, and expressed both CCR6 mRNA and protein. Therefore, LARC-CCR6 interaction presumably also contributes to the regulation of trafficking of monocyte-derived DCs, and utilization of TGF-beta can potentially provide a ready source of CCR6+ monocyte-derived DCs for therapeutic purposes.
尽管由CD34+祖细胞衍生的未成熟树突状细胞(DCs)表达CCR6,但最近的几项研究报告称,单核细胞衍生的未成熟DCs并不表达CCR6。我们观察到,在GM-CSF、IL-4和TGF-β1存在的情况下,由单核细胞产生的DCs始终对肝脏和激活调节趋化因子(LARC,也称为巨噬细胞炎性蛋白-3α)产生反应。这些未成熟DCs表达一类LARC的高亲和力结合位点,并表达CCR6 mRNA和蛋白。因此,LARC-CCR6相互作用可能也有助于调节单核细胞衍生DCs的迁移,并且利用TGF-β可能潜在地为治疗目的提供现成的CCR6+单核细胞衍生DCs来源。