Kyoto University · Medicine
Professor Koichiro Ohmura's research lab focuses on the immunological and genetic mechanisms underlying autoimmune arthritis, particularly rheumatoid arthritis (RA). The lab investigates the distinct immunogenetic profiles of ACPA-negative versus ACPA-positive RA, explores the developmental origins of hematopoietic and lymphoid progenitors in early embryogenesis, and examines the role of innate immune cells—especially neutrophils—in driving inflammatory arthritis through IL-17 production. A key focus is also on the unexpected role of Th2-type cytokines like IL-4 in promoting inflammatory arthritis, challenging traditional views of T-cell subset involvement in autoimmunity.
Figures are computed from collected data and may differ slightly.
ACPA-negative erosive RA is genetically distinct from ACPA-positive RA.
We investigated the developmental potential of hemopoietic progenitors in the aorta-gonad-mesonephros (AGM) region, where the definitive type hemopoietic progenitors have been shown to emerge before the fetal liver develops. By using an assay system that is able to determine the developmental potential of individual progenitors toward the T, B, and myeloid lineages, we show that not only multipotent progenitors but also progenitors committed to the T, B, or myeloid lineage already exist in this
Neutrophils are essential as a source of IL-17 in the effector phase of arthritis. The trigger of secreting IL-17 from neutrophils may be immune complex.
The K/BxN model, although not a classic Th2 disease, depends critically on IL-4. The potential of IL-4 to promote inflammatory arthritis should be considered when proposing therapies for rheumatoid arthritis aimed at biasing T cells toward IL-4 production.
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