IFN-γ, and few of these cells express CCR7, a chemokine receptor involved in homing to and migration within lymphoid tissues. Hence, Bonzo+ T cells would be expected to migrate preferentially to nonlymphoid destinations, and indeed, arthritic synovial fluid and inflamed liver are enriched for Bonzo+ T cells. As pointed out by Kim et al.(18), T cells in inflamed synovial fluid are efficient Th1 cytokine producers, so these new data suggest a role for Bonzo in T-cell homing to chronically inflamed tissues. Consistent with the preferential expression of Bonzo in Th1 cells, the authors also found that DCs prime naive T cells to express Bonzo and that Bonzo expression can be increased by IL-12 and decreased by IL-4. Moreover, Bonzo’s ligand, CXCL16, is expressed by DCs (19), suggesting the existence of a feedback mechanism to amplify Th1 cell responses.