Author/Authors :
Nicholson، نويسنده , , Ian C. and Mavrangelos، نويسنده , , Christos and Bird، نويسنده , , Daniel R.G. and Bresatz-Atkins، نويسنده , , Suzanne and Eastaff-Leung، نويسنده , , Nicola G. and Grose، نويسنده , , Randall H. and Gundsambuu، نويسنده , , Batjargal and Hill، نويسنده , , Danika and Millard، نويسنده , , Debbrah J. and Sadlon، نويسنده , , Timothy J. and To، نويسنده , , Sarah and Zola، نويسنده , , Heddy and Barry، نويسنده , , Simon C. and Krumbiegel، نويسنده , , Doreen، نويسنده ,
Abstract :
The peptidase inhibitor PI16 was shown previously by microarray analysis to be over-expressed by CD4-positive/CD25-positive Treg compared with CD4-positive/CD25-negative Th cells. Using a monoclonal antibody to the human PI16 protein, we found that PI16-positive Treg have a memory (CD45RO-positive) phenotype and express higher levels of FOXP3 than PI16-negative Treg. PI16-positive Treg are functional in suppressor assays in vitro with potency similar to PI16-negative Treg. Further phenotyping of the PI16-positive Treg revealed that the chemokine receptors CCR4 and CCR6 are expressed by more of the PI16-positive/CD45RO-positive Treg compared with PI16-negative/CD45RO-positive Treg or Th cells. PI16-positive Treg showed enhanced in vitro migration towards the inflammatory chemokines CCL17 and CCL20, suggesting they can migrate to sites of inflammation. We conclude that PI16 identifies a novel distinct subset of functional memory Treg which can migrate to sites of inflammation and regulate the pro-inflammatory response at those sites.
Keywords :
Memory Treg , Regulatory T cells , Lymphocyte migration , Peptidase inhibitor 16
