TP3: Inhibition of the interaction of the FcRn with IgG autoantibodies
Autoimmune diseases are of growing clinical relevance and treatment is long and difficult. High doses of intravenous IgG (IVIG) are used in therapy. One mechanism of action discussed for IVIG is the blockade of the FcRn receptor due to the high amounts of IgG. Normally, IgG’s are the proteins with the longest serum half-life which is mediated by binding to the FcRn. The project aims at the inhibition of the IgG FcRn interaction to promote the break-down of autoantibodies.
Anna Tomhardt received her Dr. rer. nat. degree in 07/2015.
- Projects
- Projects
- Associated projects
- MD projects
- Associated MD projects
- Concluded projects
- Concluded TP
- TP1 - Modulation of isotypes
- TP2 - Targeted fusion proteins
- TP3 - Selective FcRn inhibition
- TP4 - IL-35, Treg and EAE
- TP5 - Apoptotic cells
- TP6 - Mast cell / T cell interactions
- TP7 - Fc gamma receptors
- TP8 - IgG- and C-receptors
- TP9 - IVIG
- TP10 - HMGB1 Protein
- TP11 - IL15 / IL15Rα
- TP12 - S100 proteins
- TP13 - Treatment-refractory B cells
- TP A1 - Treatment strategies
- TP A2 - B cell inhibition
- TP A3 - IL-17 in EBA
- TP A4 - The pathophysiological role of Th17cells in Bullous pemphigoid
- TP A5 - C5a/C5aR
- TP A6 - Signals leading to glycosylated antibodies
- TP A7 - IL-16 & MIF in autoimmunity
- TP B1 - B cell transcriptome
- TP B2 - Antigen-specific T cells
- TP B3 - Metabolomics
- TP B4 - Resident plasma cells
- TP B5 - Anti-CD37 antibodies
- TP B6 - Systemic Sclerosis
- Concluded Ass.TP
- Concluded MD TP
- Concluded Ass. MD TP
- Concluded TP