ArticleNeuropathology and applied neurobiology2025
Myopathology and Immune Profile of Granulomatous Myositis in Sarcoid Myopathy.
Article in Neuropathology and applied neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- THE1 repeats: Ancient endogenous retroviruses rampaging behind sarcoid myopathy.Journal of human genetics · 2026Review
- From myositis to sarcoidosis: a rare autoimmune continuum.EULAR rheumatology open · 2026Article
- Myopathology and Immune Profile of Granulomatous Myositis in Sarcoid Myopathy.Neuropathology and applied neurobiology · 2025Article
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Authors and funding
23 authors.
Funding
Abstract
aimsSarcoid myopathy (SaM) is characterised by granulomatous myositis (GM) and can overlap with inclusion body myositis (IBM), a late-onset chronic idiopathic inflammatory myopathy with a still enigmatic pathogenesis. As GM can occur in different clinical contexts, we aimed to examine the histomorphologic features and gene expression profiles in cases of definite SaM that may inform diagnostic and therapeutic considerations.
methodsWe performed a multidimensional characterisation of muscle biopsy specimens from patients with 'pure SaM' (n=17), SaM with concomitant IBM (SaM-IBM) (n=2), including histopathologic and ultrastructural analysis in addition to quantitative real-time polymerase chain reaction. Additionally, bulk RNA sequencing was performed on 38 muscle biopsy specimens from patients with SaM (including SaM-IBM) (n=30) and NGI (n=8).
resultsHistopathological analysis revealed a pattern of endomysial and perimysial granulomatous inflammation frequently extending to the fascia, endomysial fibrosis, muscle fibre atrophy, variation in muscle fibre size and capillary thickening. Findings from immunohistochemical studies established Chitinase 1 as a pure giant cell marker in SaM. On a subcellular level, 'pure SaM' was characterised by focal accumulation of large swollen mitochondria with rare cristae but an absence of irregular cristae. Transcriptomic analysis of patients with SaM confirmed markedly elevated expression of both type 1 and type 2 human leukocyte antigen molecules. Macrophage activity markers were highly elevated. Consistent with histologic findings, CHIT1 was specifically overexpressed in SaM samples but not in 'pure IBM' muscle biopsy specimens.
conclusionsSaM is characterised by a stereotypical appearance at the histopathologic level and disease-specific immune dysregulation that involves macrophage function and maturation. SaM-IBM represents a noteworthy overlap syndrome that shares multiple dysregulated immune pathways with 'pure SaM'.
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