Sindhu Chandran, Joey Leung, Alexander Vu, Karim Lee, Mark Fitch, Jonathan H. Esensten, Brian R. Shy, Amy Putnam, Angela Lares, Luis A. Acevedo, Vinh Nguyen, Weihong Liu, Brian Armstrong, Zoltán Lászik, Roslyn B. Mannon, John J. Friedewald, Abhijit S. Naik, Scott Davis, Minnie Sarwal, Marc K. Hellerstein, Megan Morsheimer, Julia Goldstein, Qizhi Tang, Flavio Vincenti
Regulatory T cells (Tregs) can reverse inflammation in animal models. We conducted a randomized controlled clinical trial of Treg therapy in kidney transplant recipients with subclinical graft inflammation (NCT02711826). The primary endpoint was the change in graft inflammation on a follow-up biopsy 6 months after Treg infusion. The trial accrued 8 control group participants and 7 polyclonal Treg group participants; the latter received 400 × 10 6 to 1 × 10 9 polyclonally expanded Tregs without adverse events. Graft inflammation decreased substantially in both groups at 6 months; however, the degree of change was not significantly different between the groups. The peak of infused Tregs in circulation correlated positively with the pre-existing circulating CD4 + T cell numbers, suggesting that Treg engraftment was limited by the size of the endogenous CD4 + T cell compartment. Infused Tregs were detected in 14-day postinfusion biopsies, albeit at lower frequencies than in circulation. Unlike prior experiences, some infused Tregs emerged among non-Treg CD4 + T cells in 4 participants; these patients had higher concentrations of serum cytokines, indicative of more systemic inflammation. The study failed to show the efficacy of polyclonal Tregs due to self-resolving graft inflammation but identified the importance of monitoring Treg product identity and their stability and trafficking after infusion.