Goodarzi Katayoon, Goodarzi Mahmoud, Tager Andrew M, Luster Andrew D, von Andrian Ulrich H
Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nat Immunol. 2003 Oct;4(10):965-73. doi: 10.1038/ni972. Epub 2003 Aug 31.
Leukotriene B4 (LTB4) is a potent chemoattractant for myeloid leukocytes, which express BLT1, the high-affinity receptor for LTB4. We report here that BLT1 is induced substantially in CD8+ effector T cells and at lower amounts in CD8+ central memory T cells. LTB4 elicited BLT1-dependent chemotaxis in effector cells, but not in naive or central memory cells. Intravital microscopy showed that BLT1 signaling induced rapid integrin-mediated arrest of rolling effector and central memory cells in postcapillary venules. In competitive homing experiments, wild-type effector cells were three times more efficient at migrating to the inflamed peritoneal cavity than were BLT-deficient effector cells. These results identify LTB4-BLT1 as a potent nonchemokine pathway for cytotoxic effector cell traffic.
白三烯B4（LTB4）是一种对髓样白细胞有强大趋化作用的物质，这些白细胞表达BLT1，即LTB4的高亲和力受体。我们在此报告，BLT1在CD8 +效应T细胞中大量诱导表达，在CD8 +中枢记忆T细胞中表达量较低。LTB4在效应细胞中引发了依赖BLT1的趋化作用，但在初始或中枢记忆细胞中则没有。活体显微镜检查显示，BLT1信号传导诱导整合素介导的效应细胞和中枢记忆细胞在毛细血管后微静脉中快速滚动停滞。在竞争性归巢实验中，野生型效应细胞迁移至炎症腹膜腔的效率是BLT缺陷型效应细胞的三倍。这些结果表明LTB4 - BLT1是细胞毒性效应细胞运输的一条强大的非趋化因子途径。
