Research

Current work

PD-1–PD-L1 signaling in neonatal heart regeneration (2024, Nature Cardiovascular Research 3(3), 389–402)

In this work, I show that the PD-1–PD-L1 immune checkpoint pathway is highly active in the neonatal heart and is required for successful regeneration after myocardial infarction. Disruption of this pathway alters γδ T cell behavior, promoting autoreactive features, excessive inflammation, and fibrotic repair. These findings establish that neonatal heart regeneration does not simply occur in the setting of an immature immune system, but instead depends on active immune regulation that keeps the injury response compatible with regeneration.

A γδT17–IL-17A axis supports neonatal heart regeneration (2026, Cell Reports 45(10), 118100)

In this work, I characterize a population of γδT17 cells that accumulates in the injured heart specifically during the regenerative window and promotes regeneration through IL-17A. Mechanistically, γδT17-derived IL-17A acts primarily on myeloid cells to initiate a rapid, self-limited inflammatory response that supports injury resolution. This study links immune development to regenerative competence by showing that the neonatal heart can transiently engage a specialized immune population that is largely absent from the later injury response. It also shows that inflammatory signaling is not inherently detrimental to regeneration: when appropriately timed and rapidly resolved, it can actively support tissue repair.

Active funding

T cell-mediated regulation of mouse neonatal heart regeneration. American Heart Association, October 2025 – October 2028 (Award No. 25CDA1454364). This project studies how neonatal γδ T cells and IL-17A support heart regeneration and whether IL-17A can improve repair after the regenerative window closes.