Researchers have identified a specific immune-fibroblast interaction that appears to drive chronic inflammation in primary Sjögren disease, offering a potential new direction for treatment research. The findings, reported by Tokushima University and published in Nature Communications on May 12, 2026, suggest that the disease is sustained not only by abnormal immune activity but also by a harmful partnership with tissue-resident fibroblasts.
A closer look at the cells behind persistent inflammation
Sjögren disease is an autoimmune condition characterized by dry mouth and dry eyes, and it can also cause broader systemic complications. In the new study, researchers focused on CD4+ T cells and found that CD153+CD4+ T cells directly interact with CD30+ fibroblasts in the salivary glands. According to the report, this interaction promotes fibroblast activation, proliferation, and the production of inflammatory chemokines, helping create a microenvironment that supports ongoing inflammation and tissue damage.
The team used a mouse model of primary Sjögren disease and applied high-resolution single-cell RNA sequencing and T cell receptor sequencing to salivary gland cells. They found that the CD153+CD4+ T cell–CD30+ fibroblast axis drives the recruitment and accumulation of immune cells and supports the formation and maintenance of tertiary lymphoid structure-like tissues.
What the study suggests for future therapies
The researchers reported that removing CD153 on CD4+ T cells or neutralizing fibroblast-derived chemokines reduced immune-cell infiltration and significantly halted autoimmune-like pathology in the mouse model. They also found that patients with primary Sjögren disease show a similar increase in CD153+CD4+ T cells and CD30+ fibroblasts, with this axis correlating with disease severity.
That parallel in human patients strengthens the therapeutic relevance of the findings, although the work remains preclinical. The authors argue that the newly identified cellular interaction could serve as both a biomarker and a treatment target, with potential implications beyond Sjögren disease, including rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, and other chronic inflammatory disorders associated with fibrosis. More details about the research can be found at News Medical and the underlying journal reference at Nature Communications.
For UK clinicians and researchers, the study adds to a growing body of work showing that autoimmune disease progression may depend as much on tissue-level interactions as on immune activation alone. If confirmed in further studies, the CD153-CD30 pathway could help shape more precise strategies for slowing disease progression and protecting glandular tissue.
