New to MyHealth?
Manage Your Care From Anywhere.
Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.
ALREADY HAVE AN ACCESS CODE?
DON'T HAVE AN ACCESS CODE?
NEED MORE DETAILS?
MyHealth for Mobile
T cells expressing chimeric antigen receptor promote immune tolerance.
T cells expressing chimeric antigen receptor promote immune tolerance. JCI insight Pierini, A. n., Iliopoulou, B. P., Peiris, H. n., Pérez-Cruz, M. n., Baker, J. n., Hsu, K. n., Gu, X. n., Zheng, P. P., Erkers, T. n., Tang, S. W., Strober, W. n., Alvarez, M. n., Ring, A. n., Velardi, A. n., Negrin, R. S., Kim, S. K., Meyer, E. H. 2017; 2 (20)Abstract
Cellular therapies based on permanent genetic modification of conventional T cells have emerged as a promising strategy for cancer. However, it remains unknown if modification of T cell subsets, such as Tregs, could be useful in other settings, such as allograft transplantation. Here, we use a modular system based on a chimeric antigen receptor (CAR) that binds covalently modified mAbs to control Treg activation in vivo. Transient expression of this mAb-directed CAR (mAbCAR) in Tregs permitted Treg targeting to specific tissue sites and mitigated allograft responses, such as graft-versus-host disease. mAbCAR Tregs targeted to MHC class I proteins on allografts prolonged islet allograft survival and also prolonged the survival of secondary skin grafts specifically matched to the original islet allograft. Thus, transient genetic modification to produce mAbCAR T cells led to durable immune modulation, suggesting therapeutic targeting strategies for controlling alloreactivity in settings such as organ or tissue transplantation.
View details for PubMedID 29046484