Role of NR4A2 in pathogenic Th cells in autoimmune diseases

2018 Fiscal Year Final Research Report

• Project/Area Number: 17K16135
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurology
• Research Institution: National Center of Neurology and Psychiatry
• Principal Investigator: Raveney Ben 国立研究開発法人国立精神・神経医療研究センター, 神経研究所 免疫研究部, 科研費研究員 (70795385)
• Project Period (FY): 2017-04-01 – 2019-03-31
• Keywords: Immunology / Autoimmune diseases / T cells / Th17

Outline of Final Research Achievements

The autoimmune disease multiple sclerosis (MS) occurs when immune cells enter the brain and spine, become activated, and cause damage to self-tissues, leading to peripheral and neurological disabilities. Previously, we found that a particular gene, called NR4A2, was increased in immune cells in the blood of MS patients. In this study, we investigated how this NR4A2 gene was involved in the activation of T helper cells, a type of immune cells strongly associated with damage in MS disease, although currently the nature of these T cells that cause disease is hotly debated.
Our results showed that NR4A2 controls the type of response that T helper cells make during the initiation of autoimmune disease whey they become activated in brain/spine tissues. In particular, we discovered that NR4A2 determines if T helper cells become a pathogenic cells type, which cause damage in MS-like diseases and that these damage-associated T cells expressed novel features the allow targeting for treatment.

Free Research Field

Autoimmunity

Academic Significance and Societal Importance of the Research Achievements

This study provides new information about features of authentic damage-associated T cells in autoimmune disease. This will aid future study of the process these cells are involved in and increase understanding of cellular immunology in diseased tissues as well as providing new targets for treatment.