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This review aims to evaluate taurine's potential effects on systemic lupus erythematosus and identify knowledge gaps.

March 26, 2026Amino Acids0 citationsOpen Access

Taurine supplementation and systemic lupus erythematosus in preclinical studies: a systematic review of clinical outcomes and underlying mechanisms

AMAida Malek Mahdavi ZJZeinab JavadivalaTabriz University of Medical Sciences NONiloufar OroojiTabriz University of Medical Sciences

Key Points

This review aims to evaluate taurine's potential effects on systemic lupus erythematosus and identify knowledge gaps.
Conducted a systematic review of preclinical studies on taurine and systemic lupus erythematosus.
Search included multiple databases and utilized alerts for new publications.
Filtered articles based on strict inclusion criteria, ultimately identifying six relevant preclinical studies.
Five studies reported taurine improving clinical parameters and reducing inflammatory markers.
Taurine enhanced regulatory T cells and increased anti-inflammatory cytokines.
One study found taurine worsened SLE progression, indicating complex effects.

Abstract

Taurine (Tau) is a sulfur-containing amino acid that has therapeutic roles in several diseases, including inflammatory conditions. The involvement of Tau in modulating systemic lupus erythematosus (SLE) autoimmunity has been indicated in preclinical models, but reports are contradictory. This systematic review aimed to summarize current research regarding the potential role of Tau in SLE, to notice knowledge gaps, and to offer suggestions for the way ahead. The literature search was carried out using PubMed, Scopus, Web of Science, and Google Scholar databases until October 2025. Search alert services were also applied to notice related papers published after the primary search. All studies investigating the effects of Tau in SLE that met the inclusion criteria were eligible. Out of 77 articles initially found, only six preclinical studies (animal and in-vitro) were eligible, and no qualified clinical study was identified. Five studies indicated that Tau was helpful in improving clinical parameters, decreasing T helper 1 (Th1) and Th17 cells and inflammatory mediators (e.g., tumor necrosis factor-α, C-reactive protein, and inducible nitric oxide synthase), removing reactive oxygen species and decreasing oxidative markers like malondialdehyde, increasing regulatory T (Treg) and Th2 cells and anti-inflammatory interleukin-4 and interleukin-10 cytokines, increasing antioxidant enzymes superoxide dismutase and glutathione peroxidase, and inhibiting both FAS- and mitochondrial-dependent apoptotic signaling components. However, only one preclinical study reported that Tau aggravated SLE progression characterized by increased generation of type I interferons, enhanced autoantibodies and proteinuria, further lymphocyte activation, and critical nephritis. The current review provides evidence about the role of Tau in SLE and highlights the importance of further well-designed clinical trials to confirm these results, establish optimal dose and assess safety and long-term efficacy.

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