京都大学 · 医学
大村孝一郎教授の研究室では、自己免疫疾患、特に rheumatoid arthritis（RA）の発症メカニズムに焦点を当てた基礎研究を行っています。ACPA陽性と陰性のRAが異なる遺伝的背景を持つこと、胎児期の造血幹細胞の多様な分化能が免疫細胞の起源を解明する手がかりとなること、ニュートロフィルがIL-17を産生する重要な役割を果たすこと、そしてIL-4が炎症性関節炎に与える影響といった、免疫細粒球・自己免疫反応の制御機構を分子・細胞レベルで解明しています。特に、自己抗体や免疫複合体が炎症を引き起こすメカニズムの解明を目指しています。
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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