In the steady state, interaction between T cells and antigen-presenting dendritic cells (DCs) leads to T cell tolerance. To examine the role of DC regulated peripheral tolerance in a model autoimmune disease, we delivered an encephalitogenic oligodendrocyte glycoprotein (MOG) peptide to DCs in vivo. We found that targeting MOG peptide to DCs resulted in a novel form of peripheral T cell tolerance that was sufficiently profound to prevent autoimmune experimental acute encephalomyelitis (EAE). The tolerized T cells were severely impaired in specific secondary responses to antigen in vivo but they were not intrinsically anergic since they remained highly responsive to T cell receptor (TCR) stimulation in vitro. The mechanism that mediates this dynamic antigen-specific T cell unresponsiveness differs from previously described forms of tolerance in that it requires that DCs induce CD5 expression on activated T cells.
Hawiger, D., Masilamani, R. F., Bettelli, E., Kuchroo, V. K., & Nussenzweig, M. C. (2004). Immunological unresponsiveness characterized by increased expression of CD5 on peripheral T cells induced by dendritic cells in vivo. Immunity, 20(6), 695–705. https://doi.org/10.1016/j.immuni.2004.05.002