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Oyoshi, Michiko

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Oyoshi

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Michiko

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Oyoshi, Michiko

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2012 - 20162

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Author's Publications: search.filters.isAuthorOfPublication.35023a4b-a4c8-4724-b1f7-da597fa509f7

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    Leukotriene B4-Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation
    (Elsevier BV, 2012) Oyoshi, Michiko; He, Rui; Li, Yitang; Mondal, Subhanjan; Yoon, Juhan; Afshar, Roshi; Chen, Mei; Lee, David M.; Luo, Hongbo; Luster, Andrew; Cho, John S.; Miller, Lloyd S.; Larson, Allison; Murphy, George; Geha, Raif
    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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    IL-23 induced in keratinocytes by endogenous TLR4 ligands polarizes dendritic cells to drive IL-22 responses to skin immunization
    (The Rockefeller University Press, 2016) Yoon, Juhan; Leyva-Castillo, Juan; Wang, Guoxing; Galand, Claire; Oyoshi, Michiko; Kumar, Lalit; Hoff, Sabine; He, Rui; Chervonsky, Alexander; Oppenheim, Joost J.; Kuchroo, Vijay; van den Brink, Marcel R.M.; Malefyt, Rene De Waal; Tessier, Philippe A.; Fuhlbrigge, Robert; Rosenstiel, Philip; Terhorst, Cox; Murphy, George; Geha, Raif
    Atopic dermatitis (AD) is a Th2-dominated inflammatory skin disease characterized by epidermal thickening. Serum levels of IL-22, a cytokine known to induce keratinocyte proliferation, are elevated in AD, and Th22 cells infiltrate AD skin lesions. We show that application of antigen to mouse skin subjected to tape stripping, a surrogate for scratching, induces an IL-22 response that drives epidermal hyperplasia and keratinocyte proliferation in a mouse model of skin inflammation that shares many features of AD. DC-derived IL-23 is known to act on CD4+ T cells to induce IL-22 production. However, the mechanisms that drive IL-23 production by skin DCs in response to cutaneous sensitization are not well understood. We demonstrate that IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4+ T cells that mediates epidermal thickening. We also show that IL-23 is released in human skin after scratching and polarizes human skin DCs to drive an IL-22 response, supporting the utility of IL-23 and IL-22 blockade in AD.