Tager Andrew M, Bromley Shannon K, Medoff Benjamin D, Islam Sabina A, Bercury Scott D, Friedrich Erik B, Carafone Andrew D, Gerszten Robert E, Luster Andrew D
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
Nat Immunol. 2003 Oct;4(10):982-90. doi: 10.1038/ni970. Epub 2003 Aug 31.
Leukotriene B4 (LTB4) was originally described as a potent lipid myeloid cell chemoattractant, rapidly generated from innate immune cells, that activates leukocytes through the G protein-coupled receptor BLT1. We report here that BLT1 is expressed on effector CD4+ T cells generated in vitro as well as in vivo when effector T cells migrate out of the lymphoid compartment and are recruited into peripheral tissues. BLT1 mediated LTB4-induced T helper type 1 (T(H)1) and T(H)2 cell chemotaxis and firm adhesion to endothelial cells under flow, as well as early CD4+ and CD8+ T cell recruitment into the airway in an asthma model. Our findings show that the LTB4-BLT1 pathway is involved in linking early immune system activation and early effector T cell recruitment.
白三烯B4(LTB4)最初被描述为一种强大的脂质髓样细胞趋化因子,由天然免疫细胞快速产生,通过G蛋白偶联受体BLT1激活白细胞。我们在此报告,当效应T细胞从淋巴区室迁移出来并被招募到外周组织时,BLT1在体外和体内产生的效应CD4+T细胞上表达。在哮喘模型中,BLT1介导LTB4诱导的1型辅助性T(Th1)细胞和Th2细胞趋化以及在流动状态下与内皮细胞的牢固黏附,以及早期CD4+和CD8+T细胞向气道的募集。我们的研究结果表明,LTB4-BLT1途径参与连接早期免疫系统激活和早期效应T细胞募集。