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Article
Nature Immunology  4, 965 - 973 (2003)
Published online: 31 August 2003; | doi:10.1038/ni972

Leukotriene B4 and BLT1 control cytotoxic effector T cell recruitment to inflamed tissues

Katayoon Goodarzi1, Mahmoud Goodarzi1, Andrew M Tager2, Andrew D Luster2 & Ulrich H von Andrian1

1  Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.

2  Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.

Correspondence should be addressed to Ulrich H von Andrian uva@cbr.med.harvard.edu
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.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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