T cell receptor revision and immune repertoire changes in autoimmune diseases

Abstract

Autoimmune disease (AID) is a condition in which the immune system breaks down and starts to attack the body. Some common AIDs include systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes mellitus and so forth. The changes in T-cell receptor (TCR) repertoire have been found in several autoimmune diseases, and may be responsible for the breakdown of peripheral immune tolerance. In this review, we discussed the processes of TCR revision in peripheral immune environment, the changes in TCR repertoire that occurred in various AIDs, and the specifically expanded T cell clones. We hope our discussion can provide insights for the future studies, helping with the discovery of disease biomarkers and expanding the strategies of immune-targeted therapy.

Highlights

• Restricted TCR repertoire and biased TCR-usage are found in a variety of AIDs.

• TCR repertoire shows tissue specificity in a variety of AID diseases.

• The relationship between TCR repertoire diversity and disease activity is still controversial in AIDs.

• Dominant TCR clonotypes may help to discover new disease biomarkers and expand the strategies of immune-targeted therapy.

Keywords:

• Autoimmune disease
• clonal expansion
• immune repertoire
• immune-targeted therapy
• T-cell receptor

Acknowledgment

We thank all the authors of those included studies for their useful results.

Declaration of interest

The authors declare that they have no conflict of interest.

Additional information

Funding

The present work was supported by grants from the Science and Technology Development Fund of Pudong New District Minsheng Scientific Research (Medical and Health) Project (No. PKJ2018-Y39), the National Natural Science Foundation of China (No. 81800696, 81873636), Talent Youth Cultivation Plan of Pudong New District (No. PWRq2020-11), Shanghai Medical Key Specialty (No. ZK2019C09) and “Top-100 Talent Cultivation Plan” of Shanghai University of Medicine and Health Sciences (No. B3-0200-20-311008-30).