Journal
IMMUNITY
Volume 37, Issue 4, Pages 747-758Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2012.06.018
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Funding
- Atopic Dermatitis Research Network National Institutes of Health/National Institute of Allergy and Infectious Diseases [HHSN272201000020C]
- U.S. Public Health Service [AR-047417, AI 065858-03, HL-085100, AI-076471, HL-092020, GM-076084]
- American Cancer Society [AI-050892, AI-040618, R01 AI078910, T32 AR058921, R24 CA92865]
- Boston Children's Hospital Faculty Career Development Fellowship
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Scratching triggers skin flares in atopic dermatitis. We demonstrate that scratching of human skin and tape stripping of mouse skin cause neutrophil influx. In mice, this influx was largely dependent on the generation of leukotriene B4 (LTB4) by neutrophils and their expression of the LTB4 receptor BLT1. Allergic skin inflammation in response to epicutaneous (EC) application of ovalbumin to tape-stripped skin was severely impaired in Ltb4r1(-/-) mice and required expression of BLT1 on both T cells and non-T cells. Cotransfer of wild-type (WT) neutrophils, but not neutrophils deficient in BLT1 or the LTB4-synthesizing enzyme LTA4H, restored the ability of WT CD4(+) effector T cells to transfer allergic skin inflammation to Ltb4r1(-/-) recipients. Pharmacologic blockade of LTB4 synthesis inhibited allergic skin inflammation elicited by cutaneous antigen challenge in previously EC-sensitized mice. Our results demonstrate that a neutrophil-T cell axis reliant on LTB4-BLT1 interaction is required for allergic skin inflammation.
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