当细菌侵入身体时，免疫细胞会迅速出现在感染区与“敌人”斗争，但是，当细菌被消灭后，这些免疫细胞如何撤退呢？研究人员在4月号的《自然—免疫学》上报告说：免疫细胞从血液中的撤退需要一种以上的分子。新发现也许有助于研究人员寻找治疗炎症疾病的靶标。
淋巴细胞是一种免疫细胞，它们以与血液流动相同的速度在血管内穿梭。当身体被感染或受伤时，淋巴细胞迅速聚集到受伤点，因此，它们在任务完成后也需要撤离血管。淋巴细胞使用一种L-选择蛋白(L-selectin)来识别和抓住特定类型的复合糖蛋白——O-glycans，O-glycans 位于受感染血管壁。
Minoru Fukuda和同事发现，小鼠的淋巴细胞也能识别N-glycans糖蛋白发出的撤离信号。人类的淋巴细胞是否也具有同样的识别和撤离功能呢？这有待研究人员进一步探索。如果人类的淋巴确实具有类似功能，研究炎症疾病治疗方法的科学家们就需要寻找更多的指示淋巴细胞撤离的靶标。
部分英文原文：
Published online: 4 March 2007; | doi:10.1038/ni1442
Critical functions of N-glycans in L-selectin-mediated lymphocyte homing and recruitment
Junya Mitoma1, 6, 7, Xingfeng Bao1, 7, Bronislawa Petryanik2, Patrick Schaerli3, Jean-Marc Gauguet3, Shin-Yi Yu4, Hiroto Kawashima1, Hideo Saito1, Kazuaki Ohtsubo5, Jamey D Marth5, Kay-Hooi Khoo4, Ulrich H von Andrian3, John B Lowe2 & Minoru Fukuda1
1 Glycobiology Program, Cancer Research Center, Burnham Institute for Medical Research, La Jolla, California 92037, USA.
2 Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
3 CBR Institute for Biomedical Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
4 Institute of Biological Chemistry, Academia Sinica, Taipei 11529, Taiwan.
5 Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, California 92093, USA.
6 Present address: Division of Glyco-Signal Research, Institute of Molecular Biomembrane and Glycobiology, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba, Sendai, Miyagi 981-8558, Japan.
7 These authors equally contributed to this work.
Correspondence should be addressed to Minoru Fukuda minoru@burnham.org
Lymphocyte homing is mediated by specific interaction between L-selectin on lymphocytes and the carbohydrate ligand 6-sulfo sialyl Lewis X on high endothelial venules. Here we generated mice lacking both core 1 extension and core 2 branching enzymes to assess the functions of O-glycan-borne L-selectin ligands in vivo. Mutant mice maintained robust lymphocyte homing, yet they lacked O-glycan L-selectin ligands. Biochemical analyses identified a class of N-glycans bearing the 6-sulfo sialyl Lewis X L-selectin ligand in high endothelial venules. These N-glycans supported the binding of L-selectin to high endothelial venules in vitro and contributed in vivo to O-glycan-independent lymphocyte homing in wild-type and mutant mice. Our results demonstrate the critical function of N-glycan-linked 6-sulfo sialyl Lewis X in L-selectin-dependent lymphocyte homing and recruitment.
