Malý P, Thall A, Petryniak B, Rogers C E, Smith P L, Marks R M, Kelly R J, Gersten K M, Cheng G, Saunders T L, Camper S A, Camphausen R T, Sullivan F X, Isogai Y, Hindsgaul O, von Andrian U H, Lowe J B
Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor 48109-0650, USA.
Cell. 1996 Aug 23;86(4):643-53. doi: 10.1016/s0092-8674(00)80137-3.
alpha(1,3)Fucosylated oligosaccharides represent components of leukocyte counterreceptors for E- and P-selectins and of L-selectin ligands expressed by lymph node high endothelial venules (HEV). The identity of the alpha(1,3)fucosyltransferase(s) required for their expression has been uncertain, as has a requirement for alpha(1,3)fucosylation in HEV L-selectin ligand activity. We demonstrate here that mice deficient in alpha(1,3) fucosyltransferase Fuc-TVII exhibit a leukocyte adhesion deficiency characterized by absent leukocyte E- and P-selectin ligand activity and deficient HEV L-selectin ligand activity. Selectin ligand deficiency is distinguished by blood leukocytosis, impaired leukocyte extravasation in inflammation, and faulty lymphocyte homing. These observations demonstrate an essential role for Fuc-TVII in E-, P-, and L-selectin ligand biosynthesis and imply that this locus can control leukocyte trafficking in health and disease.
α(1,3)岩藻糖基化寡糖是白细胞针对E-选择素和P-选择素的反受体以及淋巴结高内皮微静脉（HEV）表达的L-选择素配体的组成成分。其表达所需的α(1,3)岩藻糖基转移酶的身份尚不确定，HEV L-选择素配体活性中对α(1,3)岩藻糖基化的需求也不明确。我们在此证明，缺乏α(1,3)岩藻糖基转移酶Fuc-TVII的小鼠表现出白细胞黏附缺陷，其特征为白细胞缺乏E-和P-选择素配体活性以及HEV L-选择素配体活性不足。选择素配体缺乏的表现为血白细胞增多、炎症中白细胞渗出受损以及淋巴细胞归巢异常。这些观察结果证明了Fuc-TVII在E-、P-和L-选择素配体生物合成中的重要作用，并表明该基因座可在健康和疾病状态下控制白细胞的转运。
