Leukotriene B4-Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation

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Leukotriene B4-Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation

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Title: Leukotriene B4-Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation
Author: Oyoshi, Michiko K.; He, Rui; Li, Yitang; Mondal, Subhanjan; Yoon, Juhan; Afshar, Roshi; Chen, Mei; Lee, David M.; Luo, Hongbo; Luster, Andrew David; Cho, John S.; Miller, Lloyd S.; Larson, Allison; Murphy, George Francis; Geha, Raif Salim

Note: Order does not necessarily reflect citation order of authors.

Citation: Oyoshi, Michiko K., Rui He, Yitang Li, Subhanjan Mondal, Juhan Yoon, Roshi Afshar, Mei Chen, et al. 2012. “Leukotriene B4-Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation.” Immunity 37 (4) (October): 747–758. doi:10.1016/j.immuni.2012.06.018. http://dx.doi.org/10.1016/j.immuni.2012.06.018.
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Abstract: 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.
Published Version: doi:10.1016/j.immuni.2012.06.018
Other Sources: http://www.ncbi.nlm.nih.gov/pubmed/23063331
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13349728
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