Involvement of neutrophil homing in MDS environment formation

2023 Fiscal Year Final Research Report

• Project/Area Number: 19K08820
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 54010:Hematology and medical oncology-related
• Research Institution: Fukushima Medical University
• Principal Investigator: Shikama Yayoi 福島県立医科大学, 医学部, 教授 (40291562)
• Co-Investigator(Kenkyū-buntansha): 橋本 優子 福島県立医科大学, 医学部, 教授 (60305357) ; 池添 隆之 福島県立医科大学, 医学部, 教授 (80294833)
• Project Period (FY): 2019-04-01 – 2024-03-31
• Keywords: 骨髄異形成症候群 / 好中球 / homing

Outline of Final Research Achievements

Neutrophils from patients with myelodysplastic syndromes (MDS) had decreased expression of Rca1, FDG4, and DOCK8, which contributed to their reduced migratory ability; bone marrow from MDS had more neutrophil progenitors and fewer mature neutrophils, including homing aged neutrophils, than healthy controls. However, the hypothesis that the inhibitory signal for CXCL12 production provided by monocytes phagocytosing homing neutrophils is insufficient to inhibit the release of extramedullary progenitors was not fully supported.

Free Research Field

血液学、医学教育学

Academic Significance and Societal Importance of the Research Achievements

MDS患者の最大の死因が無効造血であるが、そのメカニズムは不明である。老化血球のhomingを介する新たな無効造血メカニズムの仮説を立て、証明を試みた。好中球の遊走能を制御する三つの蛋白の発現低下、それらが実際の遊走能低下に関与していること、及びMDS骨髄内の成熟好中球の減少は検証できたものの、新しいメカニズムの証明には課題が残った。