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Kei Ikeda

Researcher at Chiba University

Publications -  135
Citations -  4542

Kei Ikeda is an academic researcher from Chiba University. The author has contributed to research in topics: Rheumatoid arthritis & Internal medicine. The author has an hindex of 29, co-authored 114 publications receiving 3781 citations. Previous affiliations of Kei Ikeda include Institute of Medical Science & Chapel Allerton Hospital.

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An explanation for the apparent dissociation between clinical remission and continued structural deterioration in rheumatoid arthritis

TL;DR: Subclinical joint inflammation detected by imaging techniques explains the structural deterioration in RA patients in clinical remission who are receiving conventional therapy and reinforces the utility of imaging for the accurate evaluation of disease status and the prediction of structural outcome.
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Reduction of fatigue in Sjögren syndrome with rituximab: results of a randomised, double-blind, placebo-controlled pilot study

TL;DR: This is the first double blind, placebo-controlled, randomised pilot study of the efficacy of rituximab in reducing fatigue in Primary Sjögren syndrome to show benefit.
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IL-25 enhances allergic airway inflammation by amplifying a TH2 cell–dependent pathway in mice

TL;DR: The enforced expression of IL-25 in the lung itself failed to induce allergic airway inflammation, whereas the expression ofIL-25 significantly enhanced antigen-induced T(H)2 cytokine production, eosinophil and CD4(+) T cell recruitment, and goblet cell hyperplasia in the airways.
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Mast cells produce interleukin-25 upon FcεRI-mediated activation

TL;DR: The results suggest that mast cells may enhance TH2-type immune response by producing IL-25, a recently described T helper 2 cell–derived cytokine that belongs to the IL-17 family and induces the production of IL-4, IL-5, and IL-13 from an unidentified non–T-cell population.
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c-Maf activates the promoter and enhancer of the IL-21 gene, and TGF-β inhibits c-Maf-induced IL-21 production in CD4+ T cells

TL;DR: Results suggest that c‐Maf induces IL-21 production directly in CD4+ T cells by activating IL‐21P and the CNS‐2 enhancer and that TGF‐β suppresses c‐ Maf‐induced IL‐ 21 production in CD 4+ T Cells.