T-cell reactivity against HSP60 relates to early but not advanced atherosclerosis
Autor: | Agnes Mayr, S. Kiechl, Michaela Kind, B. Mayrl, A. Faggionato, Michael Knoflach, Johann Willeit, J.S.H. Gaston, R. van der Zee, G. Wick |
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Rok vydání: | 2006 |
Předmět: |
Male
medicine.medical_specialty Cellular immunity Carotid Artery Common Lymphocyte T-Lymphocytes Tuberculin Inflammation Cohort Studies Epidemiology medicine Humans Aged Ultrasonography biology business.industry Vascular disease Tuberculin Test Age Factors Chaperonin 60 Middle Aged medicine.disease Atherosclerosis medicine.anatomical_structure Immunology biology.protein medicine.symptom Antibody Cardiology and Cardiovascular Medicine business Tunica Intima Biomarkers Artery |
Zdroj: | Atherosclerosis. 195(2) |
ISSN: | 1879-1484 |
Popis: | Background Anti-heat-shock protein 60 (HSP60) antibody-levels have been linked to carotid atherosclerosis and cardiovascular risk in a variety of studies. The potential role of cellular immune reactions against HSP60 has so far attracted little attention in epidemiological research. Methods and results In vitro T-cell reactivity to various HSP60s and tuberculin was assessed in blood samples from a elderly subpopulation of the Bruneck study (100 men, 50–69 years) and the young participants of the ARMY study (141 men, 17–18 years), and analyzed for a potential association with common carotoid artery intima-media thickness (IMT). In vivo skin reaction against tuberculin was recorded in subjects of the Bruneck study and correlated with the in vitro proliferative response to tuberculin ( P =0.004). T-cells isolated from peripheral blood of all individuals proliferated upon stimulation with HSP60s. In multivariate linear regression analysis adjusted for standard risk factors, T-cell stimulation was significantly related to IMT in the ARMY ( P =0.005 for human HSP60 and P =0.064 for mycobacterial HSP60) but not in the Bruneck study. Conclusions T-cell reactivity against HSP60s correlated with IMT in male youngsters but not in men aged 50 and over, indicating a more prominent role of specific cellular immunity to HSP60s in the young and very early stages of atherosclerosis. |
Databáze: | OpenAIRE |
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