T cells are one of the major drivers of systemic and local inflammation in patients with autoimmune diseases. CD4+ T cells can be divided into effector and regulatory T cells. Effector T cells are important for host defense against intracellular and extracellular pathogens but can also drive inflammation and autoimmunity. Regulatory T cells maintain immune tolerance and homeostasis by suppressing effector cell responses. Deficiency of regulatory T cells, an imbalance of effector and regulatory T cell subsets as well as the ability of Treg cells to gain effector functions can lead to fatal autoimmunity. T cell plasticity is mainly regulated by epigenetic mechanisms, such as histone modifications, which imprint cell specific signatures.
The main interest of our laboratory is to understand the exact mechanisms that are important for cell stability and identity in T cell-mediated autoimmune diseases such as Systemic Lupus Erythematosus or Rheumatoid Arthritis. Ongoing projects aim to understand the epigenetic modifications of T cells under autoimmune conditions and to reprogram pathogenic T cells.