Identification of autoantigens recognized by pathogenic T cells in autoimmune arthritis

2014 Fiscal Year Final Research Report

• Project/Area Number: 24790996
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: 膠原病・アレルギー・感染症内科学
• Research Institution: Kyoto University
• Principal Investigator: ITO Yoshinaga 京都大学, 再生医科学研究所, 助教 (60614013)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 自己抗原 / 自己反応性T細胞

Outline of Final Research Achievements

T cells mediating autoimmune diseases, such as rheumatoid arthritis (RA), are difficult to characterize because they are likely to be deleted or inactivated in the thymus if the self-antigens they recognize are ubiquitously expressed. One way to obtain and analyze these autoimmune T cells is to alter T cell receptor (TCR) signaling in developing T cells to change their sensitivity to thymic negative selection, thereby allowing their thymic production. From mice thus engineered to generate T cells mediating autoimmune arthritis, we have isolated arthritogenic TCRs and characterized the self-antigens they recognized. One of them was the ubiquitously expressed 60S ribosomal protein L23a (RPL23A), with which T cells and autoantibodies from RA patients reacted. This strategy may improve our understanding of the underlying drivers of autoimmunity.

Free Research Field

免疫学