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Hajime Suto

Researcher at Juntendo University

Publications -  72
Citations -  5717

Hajime Suto is an academic researcher from Juntendo University. The author has contributed to research in topics: Immunoglobulin E & Atopic dermatitis. The author has an hindex of 33, co-authored 69 publications receiving 5324 citations. Previous affiliations of Hajime Suto include Stanford University.

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Mast Cells Enhance T Cell Activation: Importance of Mast Cell Costimulatory Molecules and Secreted TNF

TL;DR: It is found that the secretion of soluble TNF and direct cell-cell interactions between mast cell OX40L and T cell Ox40 contribute to the ability of IgE- and Ag-stimulated mouse mast cells to enhance T cell activation.
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IL-33 can promote survival, adhesion and cytokine production in human mast cells.

TL;DR: The hypothesis that IL-33 may enhance mast cell function in allergic disorders and other settings, either in the presence or absence of co-stimulation of mast cells via IgE/antigen–FcɛRI signals is supported.
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Phenotypic differences between Th1 and Th17 cells and negative regulation of Th1 cell differentiation by IL-17.

TL;DR: It is found that the expression profile of cell surface molecules on Th17 cells has more similarities to that of Th1 cells than Th2 cells, and it is confirmed that IL‐23 or IL‐17 can suppress Th1 cell differentiation in the presence of exogenous IL‐12 in vitro.
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Mast cell–expressed orphan receptor CCRL2 binds chemerin and is required for optimal induction of IgE-mediated passive cutaneous anaphylaxis

TL;DR: It is shown that the mast cell–expressed orphan serpentine receptor mCCRL2 is not required for expression of IgE-mediated mast cell-dependent passive cutaneous anaphylaxis but can enhance the tissue swelling and leukocyte infiltrates associated with such reactions in mice.
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IL-33 induces IL-13 production by mouse mast cells independently of IgE-FcεRI signals

TL;DR: It is found that IL‐33, but not IL‐1β or IL‐18, induced IL‐13 and IL‐6 production by mouse bone marrow‐derived, cultured mast cells (BMCMCs) independently of IgE, and potential roles for IL‐ 33 in mast cell‐ and Th2 cytokine‐associated immune responses and disorders are suggested.