Immunological unresponsiveness characterized by increased expression of CD5 on peripheral T cells induced by dendritic cells in vivo

154Citations
Citations of this article
76Readers
Mendeley users who have this article in their library.

Abstract

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.

Cite

CITATION STYLE

APA

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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free