Skip to main content
Article thumbnail
Location of Repository

Surveillance of Antigen-Presenting Cells by CD4+CD25+ Regulatory T Cells in Autoimmunity : Immunopathogenesis and Therapeutic Implications

By Sébastien André, David F. Tough, Sébastien Lacroix-Desmazes, Srini V. Kaveri and Jagadeesh Bayry


CD4+CD25+ regulatory T cells (Tregs) play a critical role in preventing immune aggression. One way in which Tregs exert immune surveillance activities is by modifying the function of antigen presenting cells (APCs) such as dendritic cells, macrophages, and B cells. Tregs can induce apoptosis of APCs or inhibit their activation and function, thereby regulating subsequent innate and adaptive immune responses. These actions of Tregs are mediated by both soluble factors (interleukin [IL]-10, transforming growth factor-β, perforins, granzymes) and cell-associated molecules (cytotoxic T lymphocyte antigen 4, lymphocyte activation gene-3, CD18, neuropilin-1, LFA-1/CD11a, CD39), of which cytotoxic T lymphocyte antigen 4 has a key role. However, in autoimmunity, chronically activated APCs under the influence of intracellular signaling pathways, such as phosphatidyl inositol 3 kinase, JAK-STAT, MAPK, and nuclear factor-κB pathways, can escape surveillance by Tregs, leading to the activation of T cells that are refractory to suppression by Tregs. Moreover, APCs and APC-derived inflammatory cytokines such as tumor necrosis factor, IL-6, IL-1β, and IL-23 can render Tregs defective and can also reciprocally enhance the activity of the IL-17-producing pathogenic Th17 T cell subset. Emerging knowledge of the importance of APC-Treg interactions in maintaining immune tolerance and aberrations in this cross talk in autoimmune diseases provides a rationale for therapeutic approaches specifically targeting this axis of the immune system

Topics: Review
Publisher: American Society for Investigative Pathology
OAI identifier:
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.