TRIM Expression and Its Association With Disease Activity in Systemic Lupus Erythematosus

ABSTRACT

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse manifestations, including rash, arthritis, and nephritis. Although autoantibodies are a key feature of SLE, their levels often poorly reflect disease severity, suggesting the involvement of additional contributing factors. The tripartite motif‐containing protein (TRIM) family, which regulates immunity, may play a role in SLE. Although TRIM21 is a known autoantigen, the roles of other TRIM family members remain unclear. The present study examined TRIM expression in SLE and evaluated the potential of TRIM proteins as biomarkers. TRIM expression in peripheral blood mononuclear cells was measured using reverse transcription quantitative polymerase chain reaction (PCR) and compared between patients with SLE ( n  = 33) and healthy controls ( n  = 20). Associations of TRIM expression with disease activity (active/inactive), renal involvement (nephritis/nonnephritis), clinical manifestations, and laboratory parameters were analyzed. The expression levels of several TRIM genes, specifically TRIM5 , TRIM11 , TRIM21 , and TRIM72 , were higher in patients with inactive SLE, nonnephritic disease, or low disease activity than in patients with active disease, nephritic disease, or relapsed SLE and healthy controls. The expression levels of these genes were considerably and negatively associated with clinical symptoms but not laboratory parameters. Hydroxychloroquine users exhibited higher levels of TRIM21 expression than did nonusers. Overall, specific TRIM proteins are inversely correlated with SLE disease activity and clinical phenotypes, which indicates their potential as biomarkers. Hydroxychloroquine may regulate TRIM21 expression. Further investigation into underlying mechanisms and continued TRIM monitoring are necessary to develop new SLE treatments and better assess disease progression.