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Keeping the Immune System in Balance With the Protein RelB
How does the immune system maintain the delicate balance between attacking harmful invaders and avoiding harmful overreactions? Special immune cells called regulatory T cells (Tregs) play a vital role in this process by helping to keep the immune system in check and preventing overreaction that can lead to autoimmune diseases and allergies. Now, scientists at Helmholtz Munich have identified an important protein called ReIB in this process. Expression of this protein in another cell type called dendritic cells is essential for regulating the number and function of Tregs, highlighting its significance in maintaining immune balance. The results were published in Nature Communications.
The study, led by Dr. Caspar Ohnmacht at the Institute of Allergy Research (IAF) at Helmholtz Munich, showed that when RelB is deleted in dendritic cells, Treg levels rise, offering protection against autoimmune diseases. However, the same mechanism can lead to insufficient immune responses, making it harder to fight infections, such as parasitic invasions. By identifying a specific molecular signature and specific effects on known immune-regulatory molecules in dendritic cells caused by the absence of RelB, the researchers identified a new molecular switch that controls the level of immune activity.
By elucidating the role of RelB in maintaining the immune system in balance, the team aims to develop therapies that can either enhance immune tolerance, which is crucial in autoimmune diseases, or strengthen immune defense, particularly in cases where the immune system is compromised. This discovery holds promise for novel treatment strategies that can fine-tune immune responses, offering relief for patients suffering from a wide range of immune-related conditions.
Original publication
Geiselhöringer et al. (2024): Dominant immune tolerance in the intestinal tract imposed by RelB-dependent migratory dendritic cells regulates protective type 2 immunity. Nature communications. DOI: 10.1038/s41467-024-53112-9
Funding information
This work was funded by grants from the European Research Council (ERC Starting grant, project number 716718) and the German Research Foundation (Project Number OH 282/1-2 within FOR2599, Project Number 490846870–TRR355/1 TPA05 and TPB02 and Project Number 395357507–CRC1371 TP07).
