CTLA4 is expressed on mature dendritic cells derived from human monocytes and influences their maturation and antigen presentation

We confirmed via RT-PCR and flow cytometry the natural expression of CTLA4 on mature DCs derived from human monocytes. Approximately 8% CD1a-positive cells express CTLA4 both on surface and intracellular, whereas 10% CD1a-negative cells express CTLA4 intracellularly, but little expression was observed on the cell surface. The cross-linking of CTLA4 inhibits DCs maturation and antigen presentation in vitro, but does not inhibit endocytosis.CTLA4 is expressed by DCs and plays an inhibitory role. CTLA4-expressing DCs may represent a group of regulatory DCs. Because of its wide distribution on different cell types, CTLA4 may play a general role in regulating immune responses.Dendritic cells (DCs) are sparsely distributed in tissues and the circulation, but they are nevertheless important. They function as professional antigen-presenting cells (APCs) in antigen capture, processing, and presentation to CD4+ and CD8+ T cells [1]. DCs can be produced in vitro by a number of procedures, starting from CD34+ hemopoietic progenitor cells (from peripheral blood or bone marrow) cultured with tumor necrosis factor α (TNFα) and granulocyte macrophage-colony-stimulating factor (GM-CSF), or from human blood monocytes cultured with GM-CSF, interleukin 4 (IL-4), or IL-13. Immature DCs (iDCs), which have a high capacity for antigen uptake and processing, but a low capacity to stimulate T-cell proliferation, can be further differentiated in vitro to mature DCs (mDCs), which have a high capacity for antigen presentation, by treatment with TNFα, lipopolysaccharide (LPS), IL-1, or CD40L. Many costimulatory factors are expressed by DCs and play important roles in the communication between DCs and immunocompetent cells [2,3]. The functions of DCs are also regulated by the mutual cross-talk between costimulatory molecules [3]. The additional expression of activating costimulatory molecules that favor the interaction between DCs and T cells further enhances the ability of DCs to generate antitu