Pawel Maga1, Tomasz P Mikolajczyk2, Lukasz Partyka3, Mateusz Siedlinski4, Mikolaj Maga5, Marek Krzanowski3, Krzysztof Malinowski6, Kevin Luc4, Rafal Nizankowski5, Deepak L Bhatt7, Tomasz J Guzik8. 1. Department of Angiology, Jagiellonian University Medical College, Krakow, Poland; Angio-Medcus Angiology Clinic, Krakow, Poland. 2. Department of Internal and Agricultural Medicine, Jagiellonian University Medical College, Krakow, Poland; Institute of Infection, Immunity and Inflammation, University of Glasgow, UK. 3. Angio-Medcus Angiology Clinic, Krakow, Poland. 4. Department of Internal and Agricultural Medicine, Jagiellonian University Medical College, Krakow, Poland. 5. Department of Angiology, Jagiellonian University Medical College, Krakow, Poland. 6. Institute of Public Health, Faculty of Health Sciences, Jagiellonian University Medical College, Krakow, Poland. 7. Brigham and Women's Hospital Heart & Vascular Center, Harvard Medical School, Boston, MA, USA. 8. Department of Internal and Agricultural Medicine, Jagiellonian University Medical College, Krakow, Poland; Institute of Cardiovascular and Medical Sciences, University of Glasgow, UK. Electronic address: tomasz.guzik@glasgow.ac.uk.
Abstract
AIMS: Adaptive immunity is critical in vascular remodelling following arterial injury. We hypothesized that acute changes in T cells at a percutaneous transluminal angioplasty (PTA) site could serve as an index of their potential interaction with the injured vascular wall. METHODS AND RESULTS: T cell subsets were characterised in 45 patients with Rutherford 3-4 peripheral artery disease (PAD) undergoing PTA. Direct angioplasty catheter blood sampling was performed before and immediately after the procedure. PTA was associated with an acute reduction of α/β-TcR CD8+ T cells. Further characterisation revealed significant reduction in pro-atherosclerotic CD28nullCD57+ T cells, effector (CD45RA+CCR7-) and effector memory (CD45RA-CCR7-) cells, in addition to cells bearing activation (CD69, CD38) and tissue homing/adhesion markers (CD38, CCR5). CONCLUSIONS: The acute reduction observed here is likely due to the adhesion of cells to the injured vascular wall, suggesting that immunosenescent, activated effector CD8+ cells have a role in the early vascular injury immune response following PTA in PAD patients.
AIMS: Adaptive immunity is critical in vascular remodelling following arterial injury. We hypothesized that acute changes in T cells at a percutaneous transluminal angioplasty (PTA) site could serve as an index of their potential interaction with the injured vascular wall. METHODS AND RESULTS: T cell subsets were characterised in 45 patients with Rutherford 3-4 peripheral artery disease (PAD) undergoing PTA. Direct angioplasty catheter blood sampling was performed before and immediately after the procedure. PTA was associated with an acute reduction of α/β-TcR CD8+ T cells. Further characterisation revealed significant reduction in pro-atherosclerotic CD28nullCD57+ T cells, effector (CD45RA+CCR7-) and effector memory (CD45RA-CCR7-) cells, in addition to cells bearing activation (CD69, CD38) and tissue homing/adhesion markers (CD38, CCR5). CONCLUSIONS: The acute reduction observed here is likely due to the adhesion of cells to the injured vascular wall, suggesting that immunosenescent, activated effector CD8+ cells have a role in the early vascular injury immune response following PTA in PAD patients.
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