Camilla Successfully Defends Her PhD Thesis!
Camilla Panetti has successfully defended her PhD thesis. You can find the summary below.
The Co-Inhibitory Receptor TIGIT Confers Tissue Protective Capacity to Tregs
The co-inhibitory receptor TIGIT suppresses excessive immune responses in autoimmune conditions while also restraining anti-tumor immunity. In viral infections, TIGIT alone does not affect viral control, but has been shown to limit tissue pathology. However, the underlying mechanisms are incompletely understood. We found TIGIT+ T cells to not only express an immunoregulatory, but also a tissue repair gene signature. Specifically, upon viral infection TIGIT directly drives expression of the tissue growth factor amphiregulin (Areg), which is strongly reduced in the absence of TIGIT. We identified regulatory T cells (Tregs), but not CD8+ T cells, as the critical T cell subset mediating these tissue-protective effects. In Tregs, TIGIT engagement upon TCR stimulation induces the transcription factor Blimp-1, which then promotes Areg production and tissue repair. Thus, we uncovered a novel, non-classical function of the co-inhibitory receptor TIGIT, wherein it not only limits immune pathology by suppressing the immune response, but also actively fosters tissue regeneration by inducing the tissue repair factor Areg in T cells.
