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Increased memory and decreased naïve T cells in human hypertension (1074.9)
Author(s) -
Marvar Paul,
Cruise Tom,
Hart Emma,
Burchell Amy,
Ratcliffe Laura,
Nightingale Angus,
Paton Julian
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1074.9
Subject(s) - pathogenesis , cd8 , cd3 , flow cytometry , medicine , essential hypertension , immunology , effector , endocrinology , antigen , blood pressure
Studies have revealed a role for pro‐inflammatory effector‐like CD3+ T cells in the pathogenesis of experimental hypertension. Despite these observations, our knowledge of the role that T cells and subsets of T cells (memory vs naïve) play in the development of human hypertension is unknown. We hypothesized that circulating cells of hypertensive patients exhibit a pro‐inflammatory T cell phenotype, as determined by the balance of memory (effector) versus naïve CD3+ cells. Using flow cytometry, subsets of circulating T cells and markers of antigenic memory were analyzed in male hypertensive patients and normotensive subjects. There were no differences in the overall percentage of CD3+ cells in normotensive (63.3 ± 3.7%) (n=5; mean age 34 yrs; mean systolic BP 128.6 mmHg) vs. hypertensive men (62.2 ± 5.5%) (n=6; mean age 53.5 yrs; mean systolic BP 154.7 mmHg). The percentage of CD4+ and CD8+ T cell subsets were not statistically different between groups. Further subset analysis revealed that the ratio (1.6 ± 0.3 vs 0.7 ± 0.1; P <0.05) of memory (CD45RO+CD3+) vs. naïve (CD45RA+CD3+) T cells as well as the percentage of CD8+CD62L(low) cells (70.4 ± 4.5 vs 52.8 ± 6.3; P <0.05) were increased in hypertension. These results demonstrate an imbalance in effector memory / naïve T cells in hypertensive men and provide further evidence that chronic antigen exposure may be involved in the pathogenesis of hypertension. Supported by NIH‐HL107675‐01, Marie Curie‐IIF ‐ 276147 and British Heart Foundation. Grant Funding Source : NIH‐HL107675‐01, Marie Curie‐IIF – 276147 and British Heart Foundation