Abstract
The P2X7 receptor is expressed on T cells, however knowledge of its presence and function on human CD4 + and CD8 + subsets is limited. Immunolabeling with an anti-human P2X7 monoclonal antibody and flow cytometry demonstrated that P2X7 is present on the cell-surface of peripheral blood CD4 + and CD8 + T cells. Time-resolved flow cytometry demonstrated that extracellular ATP induced ethidium + uptake into both T cell subsets. Flow cytometric measurements also demonstrated that ATP induced the rapid loss of CD62L (L-selectin) from CD4 + and CD8 + T cells. ATP-induced ethidium + uptake and CD62L shedding were dramatically impaired in CD4 + and CD8 + T cells homozygous for the Glu496Ala loss-of-function single nucleotide polymorphism in the P2RX7 gene, demonstrating that both processes were a result of P2X7 activation. In summary, these results show that both human CD4 + and CD8 + T cells express P2X7 receptors, and that ATP activation of this receptor can lead to the rapid shedding of CD62L from these cells.
Highlights
CD62L (L-selectin) is a member of the selectin family of cell adhesion molecules, and plays important roles in the recruitment and migration of leukocytes to lymphoid tissues and sites of inflammation [1]
adenosine 5’-triphosphate (ATP)-induced ethidium+ uptake and CD62L shedding were dramatically impaired in CD4+ and CD8+ T cells homozygous for the Glu496Ala loss-of-function single nucleotide polymorphism in the P2RX7 gene, demonstrating that both processes were a result of P2X7 activation
Using peripheral blood lymphocytes from subjects wild-type, heterozygous and homozygous for the Glu496Ala single nucleotide polymorphism (SNP), the current study aimed to investigate the presence of functional P2X7 receptors on human CD4+ and CD8+ T cells, and whether activation of this receptor results in CD62L shedding from these T cell subsets
Summary
CD62L (L-selectin) is a member of the selectin family of cell adhesion molecules, and plays important roles in the recruitment and migration of leukocytes to lymphoid tissues and sites of inflammation [1]. ATP-induced ethidium+ uptake and CD62L shedding were dramatically impaired in CD4+ and CD8+ T cells homozygous for the Glu496Ala loss-of-function single nucleotide polymorphism in the P2RX7 gene, demonstrating that both processes were a result of P2X7 activation. These results show that both human CD4+ and CD8+ T cells express P2X7 receptors, and that ATP activation of this receptor can lead to the rapid shedding of CD62L from these cells.
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