Journal article

DNA methylation at IL32 in juvenile idiopathic arthritis

Braydon Meyer, Raul A Chavez, Jane E Munro, Rachel C Chiaroni-Clarke, Jonathan D Akikusa, Roger C Allen, Jeffrey M Craig, Anne-Louise Ponsonby, Richard Saffery, Justine A Ellis



Juvenile idiopathic arthritis (JIA) is the most common autoimmune rheumatic disease of childhood. We recently showed that DNA methylation at the gene encoding the pro-inflammatory cytokine interleukin-32 (IL32) is reduced in JIA CD4+ T cells. To extend this finding, we measured IL32 methylation in CD4+ T-cells from an additional sample of JIA cases and age- and sex-matched controls, and found a reduction in methylation associated with JIA consistent with the prior data (combined case-control dataset: 25.0% vs 37.7%, p = 0.0045). Further, JIA was associated with reduced IL32 methylation in CD8+ T cells (15.2% vs 25.5%, p = 0.034), suggesting disease-associated changes to a T cell precursor. A..

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Funding Acknowledgements

We thank the families who kindly participated in this study. We thank the research nurses and research assistants who undertook recruitment and data entry. We acknowledge support from the Australian National Health and Medical Research Council (NHMRC), the Australian Research Council (ARC), Arthritis Australia, Rebecca L Cooper Foundation, LEW Carty Charitable Fund, ANZ Medical Research and Technologies in Victoria Fund, Lynne Quayle Charitable Trust, The Victorian State Government Operational Infrastructure Support Program, and the Murdoch Childrens Research Institute. JAE was supported by an ARC Future Fellowship. RAC was supported by an Arthritis Australia Postgraduate Scholarship. RS and ALP were supported by NHMRC Senior Research Fellowships.