東京大学 · 医学
Yutaka Osuga教授の研究室は、子宮内膜症の発症メカニズムに焦点を当て、特に免疫系の異常と内分泌系の関与を解明することを目的としています。特に、自然殺傷細胞やT・Bリンパ球の機能異常、および下垂体ホルモン受容体の機能異常が、子宮内膜症の発症にどのように関与するかを分子細胞生物学的手法を用いて解明しています。また、子宮内膜症の病態における遺伝子発現異常やサイトコイントの不均衡の解明にも取り組んでいます。
Figures are computed from collected data and may differ slightly.
Endometriosis is a disease characterized by the presence of endometriotic tissue outside the uterine cavity. Although its pathogenesis remains to be elucidated, immune status is suggested to play an important role in the initiation and the progression of the disease. In particular, immune cells in lymphoid lineage that comprised T and B lymphocytes and natural killer cells play essential roles in determining either accept or reject survival, implantation, and proliferation of endometrial and end
Endometriosis is a disease that causes the health of women of reproductive age to deteriorate. The implantation theory is the most widely accepted pathogenesis of the disease, although many points remain poorly understood concerning this theory. According to this theory, regurgitated endometrial debris has to go through various sequential events for the disease to develop. Recent studies have elucidated several aspects of these events. A remarkably reduced gene expression of GnRH II and an incre
Gonadotropin receptors are unique members of the seven-transmembrane (TM), G protein-coupled receptor family with a large extracellular (EC) sequence forming the high-affinity ligand binding domain. In a patient with Leydig cell hypoplasia, we identified a mutant LH receptor that is truncated at TM5. This protein retains limited ligand binding ability but cannot mediate cAMP responses. To study interactions between receptor fragments defective in either ligand binding or signal transduction, we
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