BMC immunology · 2026
Elevated serum TNF-α in patients with immune-mediated necrotizing myopathy correlates with muscle damage.
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Han Xingyu, Ge Huizhen, Zhang Qing, Yang Mengge, Bu Bitao
Аннотация
OBJECTIVE: This study aimed to investigate serum levels of tumor necrosis factor-alpha (TNF-α) in patients with immune-mediated necrotizing myopathy (IMNM) and to explore its correlation with disease activity.
METHODS: Serum TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). TNF-α mRNA expression in muscle tissues from IMNM patients was detected by reverse transcription quantitative real-time PCR (RT-qPCR). In vitro experiments were performed on human muscle cells stimulated with TNF-α to assess cell viability and the expression of downstream molecules.
RESULTS: Serum TNF-α levels were significantly elevated in IMNM patients compared to healthy controls (p = 0.0002). In IMNM patients, TNF-α levels showed a significant positive correlation with serum creatine kinase (CK; p = 0.0004) and lactate dehydrogenase (LDH; p = 0.0137). TNF-α mRNA was also overexpressed in muscle biopsies from patients with IMNM. In vitro, TNF-α stimulation significantly reduced muscle cell viability and upregulated the mRNA expression of downstream inflammatory mediators, including IP-10, MCP-1, IL-6, and phosphorylated p65.
CONCLUSION: Elevated serum TNF-α in IMNM patients is associated with muscle damage and may contribute to disease pathogenesis by amplifying the inflammatory response. These findings suggest that TNF-α could serve as a potential biomarker for assessing disease severity in IMNM.
METHODS: Serum TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). TNF-α mRNA expression in muscle tissues from IMNM patients was detected by reverse transcription quantitative real-time PCR (RT-qPCR). In vitro experiments were performed on human muscle cells stimulated with TNF-α to assess cell viability and the expression of downstream molecules.
RESULTS: Serum TNF-α levels were significantly elevated in IMNM patients compared to healthy controls (p = 0.0002). In IMNM patients, TNF-α levels showed a significant positive correlation with serum creatine kinase (CK; p = 0.0004) and lactate dehydrogenase (LDH; p = 0.0137). TNF-α mRNA was also overexpressed in muscle biopsies from patients with IMNM. In vitro, TNF-α stimulation significantly reduced muscle cell viability and upregulated the mRNA expression of downstream inflammatory mediators, including IP-10, MCP-1, IL-6, and phosphorylated p65.
CONCLUSION: Elevated serum TNF-α in IMNM patients is associated with muscle damage and may contribute to disease pathogenesis by amplifying the inflammatory response. These findings suggest that TNF-α could serve as a potential biomarker for assessing disease severity in IMNM.