Molecular mechanisms and control of immune cell migration to skin and mucosa

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08831
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Hirata Takako 滋賀医科大学, 医学部, 教授 (00346199)
• Research Collaborator: Nagakubo Daisuke ; Satooka Hiroki ; Sato Tomomi ; Matsui Makoto ; Nakamura Yuzuki
• Project Period (FY): 2016-10-21 – 2019-03-31
• Keywords: 炎症 / アレルギー / リンパ球 / 好中球 / ケモカイン

Outline of Final Research Achievements

The skin and mucosa are the principal barriers that play an essential role in host defense against infection, but they are also the sites where allergies are induced in response to contact with various antigens. In this research project, we investigated molecular mechanisms underlying the immune cell migration to barrier tissues. Using a mouse model of allergic rhinitis, we demonstrated that the chemokine CCL28 was upregulated in the nasal mucosa upon nasal challenge with allergen and that memory CD4+ T cells expressing CCR3 and CCR10, the receptors for CCL28, were present in the nasal mucosa. We further found that additional CCR3 ligands also play a role in the pathogenesis of allergic rhinitis.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

免疫反応時に起こる局所への細胞浸潤は、病原体を排除するのに必須の生体防御反応であるが、同時に自己免疫・アレルギーなど重大な病態の原因でもある。特に、花粉症などのアレルギー疾患は近年増加し、全人口の約2人に1人が罹患する国民病であり、有効な新規治療法の開発が望まれる。本研究成果は、アレルギー性鼻炎マウスモデルを用いて、粘膜への免疫細胞浸潤の分子機序の一端を明らかにするものであり、花粉症などのアレルギー疾患の新規治療につながることが期待される。