Somatic mutations in clonally expanded cytotoxic T lymphocytes in patients with newly diagnosed rheumatoid arthritis.
P SavolaTiina KelkkaH L RajalaA KuulialaK KuulialaS EldforsP EllonenS LagströmM LepistöT HannunenE I AnderssonR K KhajuriaT JaatinenR KoivuniemiH RepoJ SaarelaK PorkkaM Leirisalo-RepoS MustjokiPublished in: Nature communications (2017)
Somatic mutations contribute to tumorigenesis. Although these mutations occur in all proliferating cells, their accumulation under non-malignant conditions, such as in autoimmune disorders, has not been investigated. Here, we show that patients with newly diagnosed rheumatoid arthritis have expanded CD8+ T-cell clones; in 20% (5/25) of patients CD8+ T cells, but not CD4+ T cells, harbour somatic mutations. In healthy controls (n=20), only one mutation is identified in the CD8+ T-cell pool. Mutations exist exclusively in the expanded CD8+ effector-memory subset, persist during follow-up, and are predicted to change protein functions. Some of the mutated genes (SLAMF6, IRF1) have previously been associated with autoimmunity. RNA sequencing of mutation-harbouring cells shows signatures corresponding to cell proliferation. Our data provide evidence of accumulation of somatic mutations in expanded CD8+ T cells, which may have pathogenic significance for RA and other autoimmune diseases.
Keyphrases
- newly diagnosed
- rheumatoid arthritis
- induced apoptosis
- cell proliferation
- copy number
- disease activity
- dendritic cells
- genome wide
- end stage renal disease
- cell cycle arrest
- gene expression
- interstitial lung disease
- chronic kidney disease
- systemic lupus erythematosus
- prognostic factors
- cell cycle
- single cell
- mass spectrometry
- oxidative stress
- regulatory t cells
- deep learning
- single molecule
- atomic force microscopy
- idiopathic pulmonary fibrosis
- high speed