Professor Christian Hedrich MD, PhD

Examining autoinflammatory mechanisms in CNO, my group identified pro-inflammatory phenotypes of monocytes as central players in disease pathophysiology. We’ve focused on dysregulated cytokine responses of monocytes promoting bone inflammation through inflammasome activation. Our findings explain beneficial effects of current treatment options in CNO.

Psoriasis is a mixed-pattern disorder combining features from autoinflammatory and autoimmune disorders. My research group is interested in the contribution and phenotypes of TCR+CD3+CD4-CD8- (so-called double negative, DN) T cells in health and disease. Applying state-of-the-art technology, we identified effector DN T cells as major contributors to pro-inflammatory cytokine expression in the skin of patients with psoriasis. After the definition of T cell phenotypes within the DN T cell compartment, we are aiming to i) define signature cytokine expression patterns in effector DN T cells in health and disease, and ii) determine molecular mechanisms orchestrating DN T cell lineage determination.

SLE is a largely T cell-mediated autoimmune disorder that can affect most organs of the human body. In my laboratory, we are investigating transcription factor networks contributing to epigenetic alterations and effector T cell phenotype generation in SLE. We hope that our work will contribute to novel therapeutic options targeting pathological effector T cell responses in SLE and other autoimmune disorders.