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Skin-homing CD8+ T cells preferentially express GPI-anchored peptidase inhibitor 16, an inhibitor of cathepsin K.

This study sought to identify novel CD8+ T cell homing markers by studying acute graft versus host disease (aGvHD), typically involving increased T cell homing to the skin and gut. FACS-sorted skin-homing (CD8β+/CLA+), gut-homing (CD8β+/integrinβ7+), and reference (CD8β+/CLA-/integrinβ7-) T cells were compared in patients affected by cutaneous and/or gastrointestinal aGVHD. Microarray analysis, Q-PCR and flow cytometry revealed increased expression of peptidase inhibitor 16 (PI16) in skin-homing CD8+ T cells. Robust association of PI16 with skin-homing was confirmed in all types of aGvHD and in healthy controls, too. PI16 was not observed on CLA+ leukocytes other than T cells. Induction of PI16 expression on skin-homing T cells occurred independently of vitamin D3. Among skin-homing T cells, PI16 expression was most pronounced in memory-like CD45RO+/CD127+/CD25+/CD69-/granzyme-B- cells. PI16 was confined to the plasma membrane, was GPI-anchored, and was lost upon re-stimulation of memory CD8+ T cells. Loss of PI16 occurred by down-regulation of PI16 transcription, and not by PLC- or ACE-mediated shedding, or by protein recycling. Inhibitor screening and pull-down experiments confirmed that PI16 inhibits cathepsin-K, but may not bind to other skin proteases. These data link PI16 to skin-homing CD8+ T cells, and raise the possibility that PI16 may regulate cutaneous cathepsin-K. This article is protected by copyright. All rights reserved.

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