July 29, 2025Open Access

Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies

Key Points

Anti-TRIM72 autoantibodies are elevated in patients with idiopathic inflammatory myopathies, particularly in antisynthetase syndrome and immune-mediated necrotizing myopathy.
Comparative analysis revealed no significant association between the presence of anti-TRIM72 antibodies and a more severe clinical phenotype.
Patients with ASyS who tested positive for anti-TRIM72 showed better lung function compared to those who tested negative.
Demographics and other clinic features did not differ significantly based on anti-TRIM72 status in IMNM patients with anti-HMGCR.],
simple_explanation
Anti-TRIM72 autoantibodies are proteins that can harm muscle and lung function. In patients with idiopathic inflammatory myopathies, these antibodies were found in higher amounts, but they didn't link to worse health outcomes. Interestingly, some patients with these antibodies had better lung capacity. This research helps doctors understand how these autoantibodies impact patient health. 🩺
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Abstract

Tripartite motif-containing protein 72 (TRIM72) mediates tissue-repair following injury in several organs, including muscle and lung. Autoantibodies directed against TRIM72 (anti-TRIM72) have been identified in patients with idiopathic inflammatory myopathies (IIM) and disrupt TRIM72 function in vitro. We hypothesized that IIM patients positive for anti-TRIM72 antibodies would have a more severe clinical phenotype. Sera from IIM patient (antisynthetase syndrome ASyS, immune mediated necrotizing myopathy IMNM, and dermatomyositis DM) and healthy controls (HC) were included. Anti-TRIM72 autoantibodies were tested using enzyme linked immunosorbent assay. Anti-TRIM72 testing was positive if value was >2 standard deviations above the mean for HC. Clinicodemographic features were identified through chart review and compared between anti-TRIM72 positive (anti-TRIM72+) and negative (anti-TRIM72-) groups. Anti-TRIM72 levels were significantly increased in patients with ASyS and IMNM when compared to patients with DM and healthy controls. Anti-TRIM72 levels were also increased in patients expressing anti-Jo-1, anti-PL7, anti-HMGCR, anti-SRP, and anti-MDA5. In ASyS, when anti-TRIM72(+) and anti-TRIM72(-) patients were compared, there were significantly more anti-TRIM72(+) ASyS patients with normal DLCO (>75%) when compared to anti-TRIM72(-); however, there were no differences in demographic features, CK levels or FVC. In anti-HMGCR(+) IMNM, anti-TRIM72(+) was associated with a lower proportion of females, as well as older age at time of diagnosis and at time of anti-TRIM72 testing; however, there was no significant difference in other clinicodemographic features in anti-HMGCR(+) IMNM patients when anti-TRIM72(+) and anti-TRIM72(-) groups were compared. Anti-TRIM72 antibody titres are increased in patients with ASyS and IMNM. The presence of anti-TRIM72 antibodies was not associated with a more severe phenotype in ASyS or anti-HMGCR(+) IMNM, and there were more ASyS patients with normal DLCO in the anti-TRIM72(+) group.

Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies

Key Points

Abstract

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