Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Transforming growth factor beta (TGF-β) is a cytokine with complex immunomodulatory functions, implicated in the maintenance of immune tolerance and the regulation of inflammatory responses. Scientific interest in TGF-β for lupus (systemic lupus erythematosus, SLE) arises from observations that patients with SLE often exhibit impaired TGF-β signaling and reduced levels of TGF-β in immune cells. Experimental studies, primarily in animal models, have shown that increasing TGF-β activity or signaling can ameliorate disease activity by suppressing autoimmunity and inflammation. For example, TGF-β can promote the generation of regulatory T cells (Tregs) and suppress autoreactive lymphocytes, mechanisms relevant to the pathogenesis of lupus.

However, direct clinical application of TGF-β as a therapeutic agent in lupus is limited. Most evidence comes from preclinical studies, and there is currently a lack of robust, large-scale clinical trials demonstrating safety and efficacy of TGF-β supplementation or augmentation in lupus patients. Furthermore, due to TGF-β’s profibrotic potential and association with organ fibrosis, especially in kidneys (a common concern in lupus nephritis), its therapeutic use raises safety concerns.

In summary, while there is scientific rationale and some supportive preclinical evidence for targeting TGF-β pathways in lupus, clinical validation remains insufficient. Thus, the evidence ranks moderately low (2/5), reflecting promising but not yet clinically validated support for its use in lupus treatment.

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