TLR2 Is Expressed on Activated T Cells as a Costimulatory Receptor

• Published in: Proceedings of the National Academy of Sciences - PNAS 2004-03, Vol.101 (9), p.3029-3034
• Main Authors: Komai-Koma, Mousa, Jones, Louise, Ogg, Graham S., Xu, Damo, Liew, Foo Y., Moncada, Salvador
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Antigen presenting cells; Antigen-Presenting Cells - immunology; B lymphocytes; Base Sequence; Biological Sciences; Cell lines; Cultured cells; Cytokines; DNA Primers; Fetal Blood - immunology; Flow Cytometry; Gene expression; Humans; Immune system; Immunologic Memory; Immunology; Infant, Newborn; Insects; Ligands; Lymphocyte Activation - immunology; Membrane Glycoproteins - deficiency; Membrane Glycoproteins - genetics; Memory; Mice; Mice, Knockout; Polymerase Chain Reaction; Receptors; Receptors, Cell Surface - deficiency; Receptors, Cell Surface - genetics; Receptors, Cell Surface - immunology; T cell receptors; T lymphocytes; T-Lymphocytes - immunology; Toll-Like Receptor 2; Toll-Like Receptors
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.0400171101

Toll is the founder of a group of pattern recognition receptors that play a critical role in the innate immunity in Drosophila. At least 10 distinct Toll-like receptors (TLRs), recognizing pathogen-associated molecular patterns, have now been identified in humans. Most investigations on TLRs have focused on cells of the innate system. We report here that naïve human T cells expressed high levels of cell-surface TLR2 after activation by anti-T cell receptor antibody and IFN-α. Activated cells produced elevated levels of cytokines in response to the TLR2 ligand, bacterial lipopeptide. Furthermore, CD4+CD45 RO+memory T cells from peripheral blood constitutively expressed TLR2 and produced IFN-γ in response to bacterial lipopeptide, which also markedly enhanced the proliferation and IFN-γ production by CD45 RO+T cells in the presence of IL-2 or IL-15. Thus, TLR2 serves as a costimulatory receptor for antigen-specific T cell development and participates in the maintenance of T cell memory. This suggests that pathogens, via their pathogen-associated molecular patterns, may contribute directly to the perpetuation and activation of long-term T cell memory in both antigen-dependent and independent manner.