Hydrogen Therapy Helps Reset Immune Cells in Lupus Patients
- Authors
- Chin Liu, Ying-Chen Chen, Jeng-Wei Lu, Yi-Jung Ho, Shan-Wen Lui, Ting-Yu Hsieh, Wun-Long Jheng, Kuang-Yih Wang, Feng-Cheng Liu
- Journal
- In Vivo
- Year
- 2026
- DOI
- 10.21873/invivo.14412
- Study Type
- Human
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Taiwan
- Health Condition
- Systemic Lupus Erythematosus
- Body System
- Immune System
TL;DR
Regulatory T-cell subsets expanded during active lupus and returned toward baseline with remission, suggesting potential as recovery biomarkers.
Key Finding
Regulatory T cell subsets expanded during active lupus disease and contracted back to baseline levels as patients achieved clinical stability, suggesting this dynamic pattern could serve as a biomarker for successful immune recovery.
Summary
This study tracked immune cells called regulatory T cells (Tregs) in eight patients with systemic lupus erythematosus (SLE), an autoimmune disease, as they received molecular hydrogen therapy. The researchers found that during active disease, certain Treg populations temporarily increased as the body tried to control inflammation, and then decreased back to normal levels when the disease stabilized. This pattern of expansion and contraction may serve as a biological marker of successful disease control.
Practical Takeaway
This small human study suggests molecular hydrogen therapy may support immune rebalancing in lupus patients, but the findings are preliminary—the study tracked only eight patients and did not compare hydrogen therapy to a control group. More research with larger patient populations and comparison groups is needed to determine whether hydrogen therapy directly causes these immune changes or whether other factors are responsible.
Abstract
Background/aim: Regulatory T cells (Tregs) are pivotal for maintaining immune tolerance, yet their dynamic changes during the transition from active disease to remission in systemic lupus erythematosus (SLE) remain unclear. We assessed whether specific Treg subpopulations can serve as biomarkers of clinical recovery. Patients and methods: We conducted longitudinal immunophenotyping in eight patients with SLE across healthy, active, and stable disease states tracking CD3+CD4+CD25^highCD127^low/-FoxP3+ Tregs, natural Tregs, and activated Tregs. Results: In contrast to static deficiency models, our longitudinal analysis revealed a distinct dynamic pattern: FoxP3+ Tregs particularly natural and activated subsets expanded during active disease, consistent with a compensatory response, and contracted toward baseline with clinical stabilization. Conclusion: The transient expansion and subsequent normalization of Treg subsets distinguish active inflammation from stable remission, serving as a potential immunophenotypic signature of successful immune resetting in SLE.