Tregs in Tissue Repair
The Role of Tregs in Tissue Repair
Regulatory T cells (Tregs) are well known for keeping the immune system in check, helping prevent autoimmunity while also posing a challenge in cancer by suppressing anti-tumor immunity. While their immunosuppressive role has been widely studied, a growing body of research highlights an additional, less understood function: promoting tissue repair.
To understand how Tregs contribute to tissue repair, we study their responses during chronic viral infections. We have identified amphiregulin (Areg), a growth factor that helps regenerate damaged tissues, as a key player in this regard. Interestingly, it appears that the Areg response is dependent on the co-inhibitory receptor TIGIT which is traditionally associated with immune suppression. TIGIT not only dampens inflammation through inhibition of effector T cells during viral infections but also directly enhances the tissue-repair capacity of Tregs by promoting Areg production.
In addition to Areg, we are also studying the role of TGF-β, which has been linked to the tissue-repair program. Due to its high expression in Tregs, we aim to understand the role of TGF-β produced by Tregs in settings of tissue regeneration and how this response might be linked to other mediators in the tissue repair program.
Together, we are studying the pathways involving TIGIT, Areg and TGF-β that enable Tregs to go beyond immune regulation and actively contribute to tissue repair. Understanding these mechanisms could open up new therapeutic avenues, including the potential to target TIGIT in diseases marked by tissue damage.
Related Publications
Schorer M., et al., TIGIT limits immune pathology during viral infections. Nat. Comm. (2020).
