Checkpoint imbalances in autoimmunity

Antibodies are essential for protection against pathogens, but when misdirected they can drive severe autoimmune diseases. In this project, we investigate antibody-mediated autoimmune disorders affecting the central and peripheral nervous system, where pathogenic autoantibodies are suspected to play a key role.

The generation of antibody responses depends on tightly regulated interactions between B and T cells that are controlled by co-stimulatory and co-inhibitory immune checkpoint molecules. Disruption of this balance can promote chronic immune activation and autoantibody production.

Within the clinical research consortium KFO BecauseY, we dissect immune checkpoint regulation in B–T cell interactions to identify disease-driving mechanisms in antibody-associated neurological diseases. Using multimodal immune profiling and high-dimensional spatial analyses, we aim to identify biomarkers for patient stratification and explore checkpoint pathways as targets for immunotherapy.

  • Lucas Arendholz

    Postdoc

  • Dzenis Koca

    Postdoc

  • Olufemi Bolaji

  • Katrin Vogt

    Technical Assistant

  • Juliette Schöning

    Technical Assistant

  • Christine Appelt

    Technical Assistant

  • Carolin Hennig

    Student Assistant

  • Josefine Behrends

    Student Assistent

  • Killer-like receptors and GPR56 progressive expression defines cytokine production of human CD4(+) memory T cells.

    Nature Communications

  • CD96 expression determines the inflammatory potential of IL-9-producing Th9 cells.

    Proc Natl Acad Sci U S A

Sawitzki Lab

Berlin Institute of Health at Charité (BIH) 
Center of Immunomics/Translational Immunology

Luisenstraße 65 
D-10117 Berlin