2020 Fiscal Year Final Research Report
Investigation of novel JAK-STAT pathway in ulcerative colitis.
Project/Area Number |
19K17484
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 53010:Gastroenterology-related
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
Hiromichi Shimizu 東京医科歯科大学, 医学部附属病院, 特任助教 (00733875)
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Project Period (FY) |
2019-04-01 – 2021-03-31
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Keywords | 潰瘍性大腸炎 / クローン病 / JAK阻害薬 |
Outline of Final Research Achievements |
Ulcerative colitis is an idiopathic disease which causes chronic inflammation in colon. For the treatment of ulcerative colitis, anti-inflammatory agents are used such as corticosteroid, immune-modulator and biologic agents. JAK inhibitor is one of biologic agent blocking strongly pro-inflammatory JAK pathway in colonic tissue. JAK pathway has a vast cytokine-network interacting numerous other pathways, and it needs to be studied deeply and broadly. This study, using colonic tissue derived from the patients with ulcerative colitis, was aiming to investigate what kind of cells JAK inhibitor has any effects, how JAK inhibitor reduces and blocks proinflammatory response in colonic tissue, and what is the key biomarkers and/or conditions that regulate its treatment efficacy of the patients. We performed single-cell PCR analysis on organoids generated from colonic tissue derived from the patients with ulcerative colitis.
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Free Research Field |
再生医療研究
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Academic Significance and Societal Importance of the Research Achievements |
潰瘍性大腸炎の治療には、免疫制御効果を持つ副腎皮質ステロイドや免疫調節薬、分子標的薬などが用いられ、分子標的薬は炎症を引き起こす複雑なサイトカイン・ネットワークの、特異的な経路を阻害して効果を発揮する。分子標的薬は潰瘍性大腸炎治療の成績を大きく向上した一方、どのように障害された腸粘膜を治癒するのか、その作用メカニズムはよくわかっていない。本研究は、患者の臨床情報と患者由来の組織検体の解析を通じて、分子標的薬のひとつJAK阻害薬の作用メカニズムの解明と、治療有効性が規定される因子の同定を試みることで、JAK阻害薬が有効である患者の拾い上げと治療効果予測の解明を目標とした研究である。
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