潜伏期相关肽具有独立于转化生长因子-β1的体外和体内免疫效应。
Latency associated peptide has in vitro and in vivo immune effects independent of TGF-beta1.
作者信息
Ali Naeem A, Gaughan Alice A, Orosz Charles G, Baran Chris P, McMaken Sara, Wang Yijie, Eubank Timothy D, Hunter Melissa, Lichtenberger Frank J, Flavahan Nicholas A, Lawler Jack, Marsh Clay B
机构信息
Department of Internal Medicine, The Ohio State University, Columbus, Ohio, United States of America.
出版信息
PLoS One. 2008 Apr 2;3(4):e1914. doi: 10.1371/journal.pone.0001914.
Latency Associated Peptide (LAP) binds TGF-beta1, forming a latent complex. Currently, LAP is presumed to function only as a sequestering agent for active TGF-beta1. Previous work shows that LAP can induce epithelial cell migration, but effects on leukocytes have not been reported. Because of the multiplicity of immunologic processes in which TGF-beta1 plays a role, we hypothesized that LAP could function independently to modulate immune responses. In separate experiments we found that LAP promoted chemotaxis of human monocytes and blocked inflammation in vivo in a murine model of the delayed-type hypersensitivity response (DTHR). These effects did not involve TGF-beta1 activity. Further studies revealed that disruption of specific LAP-thrombospondin-1 (TSP-1) interactions prevented LAP-induced responses. The effect of LAP on DTH inhibition depended on IL-10. These data support a novel role for LAP in regulating monocyte trafficking and immune modulation.
潜伏期相关肽（LAP）与转化生长因子-β1（TGF-β1）结合，形成潜伏复合物。目前，LAP被认为仅作为活性TGF-β1的隔离剂发挥作用。先前的研究表明，LAP可诱导上皮细胞迁移，但对白细胞的影响尚未见报道。由于TGF-β1参与多种免疫过程，我们推测LAP可能独立发挥作用来调节免疫反应。在单独的实验中，我们发现LAP促进人单核细胞的趋化作用，并在迟发型超敏反应（DTHR）的小鼠模型中体内阻断炎症。这些作用不涉及TGF-β1的活性。进一步的研究表明，特定的LAP-血小板反应蛋白-1（TSP-1）相互作用的破坏可阻止LAP诱导的反应。LAP对DTH抑制的作用依赖于白细胞介素-10。这些数据支持LAP在调节单核细胞运输和免疫调节中的新作用。
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