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Thyroid lesions reach maximal severity 20 days after cell transfer, and usually resolve or progress to fibrosis by day 60 depending on the extent of thyroid damage at day 20. Our previous studies indicated that neutralization of TNF\u2010\u03b1 or FasL had no effect on G\u2010EAT induction, but neutralization of TNF\u2010\u03b1 promoted, while neutralization of FasL inhibited, G\u2010EAT resolution. TNF\u2010related apoptosis\u2010inducing ligand (TRAIL) is a member of the TNF superfamily. This study was undertaken to define the role of endogenous TRAIL in G\u2010EAT development and\/or resolution. Neutralization of endogenous TRAIL had little effect on G\u2010EAT induction, but significantly inhibited G\u2010EAT resolution and increased thyroid fibrosis. This correlated with higher expression of pro\u2010inflammatory cytokines and preferential expression of the pro\u2010apoptotic molecule TRAIL, and anti\u2010apoptotic molecules FLIP and Bcl\u2010xL on inflammatory cells in thyroids of anti\u2010TRAIL\u2010treated recipients. The results suggest that endogenous TRAIL is not required for G\u2010EAT development in recipients, but is critical for G\u2010EAT resolution. Endogenous TRAIL might promote resolution, at least in part, through modulation of the balance between pro\u2010 and anti\u2010inflammatory cytokines, and the expression pattern of pro\u2010 and anti\u2010apoptotic molecules of thyroid epithelial cells (TECs) and inflammatory cells. Copyright \u00a9 2008 Pathological Society of Great Britain and Ireland. 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