K
Koji Iijima
Researcher at Mayo Clinic
Publications - 79
Citations - 3979
Koji Iijima is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Immune system & Immunology. The author has an hindex of 26, co-authored 61 publications receiving 3289 citations. Previous affiliations of Koji Iijima include University of Rochester.
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Journal ArticleDOI
Cellular senescence mediates fibrotic pulmonary disease
Marissa J. Schafer,Thomas A. White,Koji Iijima,Andrew J. Haak,Giovanni Ligresti,Elizabeth J. Atkinson,Ann L. Oberg,Jodie Birch,Hanna Salmonowicz,Yi Zhu,Daniel L. Mazula,Robert W. Brooks,Heike Fuhrmann-Stroissnigg,Tamar Pirtskhalava,Y. S. Prakash,Tamara Tchkonia,Paul D. Robbins,Marie Christine Aubry,João F. Passos,James L. Kirkland,Daniel J. Tschumperlin,Hirohito Kita,Nathan K. LeBrasseur +22 more
TL;DR: It is demonstrated that early-intervention suicide-gene-mediated senescent cell ablation improves pulmonary function and physical health, although lung fibrosis is visibly unaltered, and fibrotic lung disease is mediated, in part, by senescent cells.
Journal ArticleDOI
IL-33–Responsive Lineage−CD25+CD44hi Lymphoid Cells Mediate Innate Type 2 Immunity and Allergic Inflammation in the Lungs
Kathleen R. Bartemes,Koji Iijima,Takao Kobayashi,Gail M. Kephart,Andrew N. J. McKenzie,Hirohito Kita +5 more
TL;DR: A subset of innate immune cells that responds to IL-33 and vigorously produces Th2-type cytokines is present in mouse lungs, which may provide a novel mechanism for type 2 immunity in the airways and induction of allergic airway diseases such as asthma.
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A novel IL-1 family cytokine, IL-33, potently activates human eosinophils.
TL;DR: IL-33 and its receptor, ST2, may play important roles in eosinophil-mediated inflammation; they may provide new therapeutic targets for controlling mucosal eOSinophilic inflammation.
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The Danger Signal, Extracellular ATP, Is a Sensor for an Airborne Allergen and Triggers IL-33 Release and Innate Th2-Type Responses
TL;DR: Airway exposure of naive mice to a common environmental aeroallergen, the fungus Alternaria alternata, induces rapid release of IL-33 into the airway lumen, followed by innate Th2-type responses, and ATP and purinergic signaling in the respiratory epithelium are critical sensors for airway exposure to airborne allergies.
Journal ArticleDOI
Group 2 innate lymphoid cells and CD4+ T cells cooperate to mediate type 2 immune response in mice
TL;DR: This work sought to investigate the capacity of ILC2s to regulate effector functions of T cells in innate lymphoid cells and found it to be able to mediate the immune pathology of asthma even without adaptive immunity.