Control of Effector CD8 ⁺ T Cell Function by the Transcription Factor <i>Eomesodermin</i>

TLDR

Activated CD8⁺ T cells are essential for defense against viruses, intracellular microbes, and tumors, yet it remains unclear whether a single transcription factor coordinates their effector functions. We demonstrate that Eomesodermin is induced in effector CD8⁺ T cells and that its overexpression drives IFN‑γ, perforin, and granzyme B production, while loss‑of‑function studies indicate it is required for full effector differentiation, suggesting Eomes complements T‑bet as a key regulatory gene in cell‑mediated immunity.

Abstract

Activated CD8 + T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8 + T cells. We now show that Eomesodermin ( Eomes ), a paralogue of T-bet , is induced in effector CD8 + T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8 + T cells, including interferon-γ (IFN-γ), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8 + T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.