We have recently shown that forced expression of CCR4 by effector T cells enhances their migration to Hodgkin tumor, so that coexpression of both CCR4 and a chimeric antigen receptor directed to the Hodgkin lymphoma (HL)–associated antigen CD30 produces better tumor control when these cells are infused intravenously in mice engrafted with human CD30/thymus and activationregulated chemokine–secreting HL. 1 In their letter to the editor, Aldinucci and colleagues point out that Hodgkin Reed-Sternberg cells also produce CCL5/Rantes in addition to other, previously reported chemokines, such as thymus and activation-regulated chemokine and macrophage-derived chemokine.

Although we agree with the suggestion by Aldinucci et al that it is therefore appropriate to consider overexpressing CCR5 (the receptor for CCL5/Rantes) in T cells to maximize tumoral migration, we chose not to do this for two reasons. First, CCL5/Rantes is constitutively expressed in normal lung, 2, 3 where it mediates T-cell transmigration from the pulmonary vasculature compartment into the interstitium. 4 Expression is increased during infection or inflammation. Hence, T cells overexpressing CCR5 could well be diverted to normal lung tissue. Because pulmonary vascular trapping of infused Tlymphocytes undoubtedly occurs even with unmodified cells, we were anxious not to further increase this process.