Keio University

Mechanism of a "vicious cycle" of autoimmunity uncovered in Sjögren's disease

Discovery may enable development of therapies that selectively target disease-causing autoimmune responses

Published: June 04, 2026
Office of Communications and Public Relations

Keio University School of Medicine

A research team at Keio University School of Medicine and JSR Corporation has uncovered a mechanism by which immune cells interact to sustain autoimmune responses in Sjögren's disease, as part of the JKiC Next-Generation Project. The team comprises Masaru Takeshita (Assistant Professor) and Yuko Kaneko (Professor) from the Division of Rheumatology at Keio University School of Medicine, Seiki Wakui (Chief Researcher) from JSR Corporation, among others.

In this study, the researchers investigated which molecules are recognized by CD4⁺ T cells infiltrating the salivary glands of patients with Sjögren's disease. By combining single-cell analysis with T-cell reporter assays, they identified CD4⁺ T cells that recognize peptides derived from the protein Ro60. Furthermore, many of these T cells exhibited characteristics of T follicular helper (Tfh) and T peripheral helper (Tph) cells, which support antibody production by B cells. The research group has previously reported that B cells infiltrating the salivary glands of patients with Sjögren's disease frequently produce antibodies against Ro60. Together with the present findings, these results indicate that CD4⁺ T cells and B cells interact to amplify immune responses against Ro60, forming what can be described as a "vicious cycle" of autoimmunity.

These findings not only contribute to a better understanding of the mechanisms underlying Sjögren's disease but also provide important insights that may lead to the development of new therapies that selectively suppress disease-causing autoimmune responses.

The results of this study was published in the American scientific journal Science Advances on June 3, 2026 (ET).    

For further information, please refer to the following PDF file.

Press Release (PDF)