Now, Anna-Lena Geiselhöringer and the team from the Mucosal Immunology group at ZAUM identified a key role for a transcription factor called RelB to control the number of Tregs in various tissues. Importantly, the team discovered that the ablation of this factor in a specific cell type called dendritic cells increases the number of Tregs dramatically. Dendritic cells are so-called antigen-presenting cells that constantly sample and present both foreign and self-antigens to T cells. In the absence of RelB, dendritic cells that just migrated to gut-draining lymph nodes showed a different expression profile including several key immunoregulatory molecules (e.g. chemokines controlling the direct cross-talk with Tregs) that in sum favor Treg accumulation. On a side note, the team also discovered a complete RelB dependency of a specific dendritic cell subset surrounding lymphoid follicles in the intestinal tract, but this absence was not responsible for the increased Treg numbers. The increased Treg numbers prevented the efficient induction of a protective Th2 response after infection with a worm parasite called Heligmosomoides polygyrus. “This finding indicates that the level of immune activity is tightly controlled by the number of Tregs and the RelB pathway in dendritic cells acts as a molecular rheostat for this process” explains PD Dr. Caspar Ohnmacht. With this knowledge in hand, there is now the possibility to influence the number of Tregs in cases of overshooting activation such allergies, autoimmune diseases or other chronic inflammatory diseases.