Author

R. Takagi

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

M. Kawano· 2 shared M. Tokano· 2 shared S. Matsushita· 2 shared A. UMEZAWA· 1 shared C. Kobori· 1 shared H. Takahashi· 1 shared K. Kishi· 1 shared M. Mori· 1 shared

Activity by Year

2021-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersImmunology

M. Kawano

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Functional and long-lived melanocytes from human pluripotent stem cells with transient ectopic expression of JMJD3

C. Kobori, R. Takagi, R. Yokomizo, S. Yoshihara, M. Mori, H. Takahashi, P. K. Javaregowda, T. Akiyama, M. S. H. Ko, K. Kishi, A. UMEZAWA

This study generates functional and long-lived melanocytes from human pluripotent stem cells using transient JMJD3 expression, showing melanogenesis and engraftability in mice.

bioRxiv · Mar 3, 2023Cell Biology

Istradefylline, an adenosine A2a receptor antagonist, ameliorates neutrophilic airway inflammation and psoriasis in mice

M. Tokano, M. Kawano, R. Takagi, S. Matsushita

This study shows that istradefylline and related inhibitors reduce IL-17A production in mouse models of neutrophilic inflammation and psoriasis.

bioRxiv · May 21, 2021Immunology

Extracellular adenosine induces hypersecretion of IL-17A by T-helper 17 cells through the adenosine A2a receptor to promote neutrophilic inflammation

M. Tokano, S. Matsushita, R. Takagi, T. Yamamoto, M. Kawano

This study shows adenosine enhances IL-17A secretion by Th17 cells via A2aR, promoting neutrophilic inflammation and suggesting A2aR antagonists as potential treatments for Th17-related autoimmune diseases.

bioRxiv · Apr 29, 2021Immunology