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Detail

Michael Bonelli

Department of Medicine III (Division of Rheumatology)
Position: Associate Professor

ORCID: 0000-0002-6122-7482
T +43 1 40400 43010
michael.bonelli@meduniwien.ac.at

Keywords

Arthritis, Rheumatoid; Epigenomics; Lupus Erythematosus, Systemic; T Cells

Research group(s)

Research interests

 My long-term research interest is the pathophysiology of immune-mediated diseases. I focused on the role of T cells and monocytes as major drivers of systemic inflammation. I published several papers in the field of Rheumatology and Immunology, which establish the role of regulatory T cells in patients with autoimmune diseases. A major interest lies within the epigenetic modifications of T cells that are responsible for cell plasticity and stability, in particular in patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus. Among other things we aim to address the effects of T cell – fibroblast interactions on the development of pathogenic T cells. Experiments are designed in the human system as well as in several arthritis models, which are dependent on the adaptive and innate immune system, to test the role of T cell subsets for the development of arthritis.

Techniques, methods & infrastructure

 To address the role of cell subsets as drivers of autoimmune diseases we have established various arthritis models, which are dependent on the innate and the adaptive immune system, including the TNF transgenic, the serum transfer arthritis model and the collagen-induced and OVA-induced arthritis model. Various in vitro culture systems allow to address the role of cell-cell interactions in patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus. ChIP-Sequencing for histone modifications as well as ATAC-sequencing in combination with RNA-sequencing aim to determine the chromatin structure and the transcriptome of pathogenic T cell subsets.

Selected publications

  1. Bonelli, M. et al., 2018. CCR6 controls autoimmune but not innate immunity-driven experimental arthritis. Journal of Cellular and Molecular Medicine, 22(11), pp.5278-5285. Available at: http://dx.doi.org/10.1111/jcmm.13783.
  2. Roychoudhuri, R. et al., 2013. BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis. Nature, 498(7455), pp.506-510. Available at: http://dx.doi.org/10.1038/nature12199.
  3. Bonelli, M. et al., 2015. Abatacept (CTLA-4Ig) treatment reduces T cell apoptosis and regulatory T cell suppression in patients with rheumatoid arthritis. Rheumatology, 55(4), pp.710-720. Available at: http://dx.doi.org/10.1093/rheumatology/kev403.
  4. Bonelli, M. et al., 2014. Helper T Cell Plasticity: Impact of Extrinsic and Intrinsic Signals on Transcriptomes and Epigenomes. Current Topics in Microbiology and Immunology, pp.279-326. Available at: http://dx.doi.org/10.1007/82_2014_371.
  5. Bonelli, M. et al., 2014. CD4+CD25-Foxp3+ T cells: a marker for lupus nephritis? Arthritis Research & Therapy, 16(2), p.R104. Available at: http://dx.doi.org/10.1186/ar4553.