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Relationship of CD 146 expression to activation of circulating T cells: exploratory studies in healthy donors and patients with connective tissue diseases
Author(s) -
Hadjinicolaou A. V.,
Wu L.,
Fang B.,
Watson P. A.,
Hall F. C.,
Busch R.
Publication year - 2013
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12151
Subject(s) - cd146 , immunology , cd28 , t cell , cd8 , il 2 receptor , biology , antigen , immune system , microbiology and biotechnology , stem cell , cd34
Summary The endothelial cell adhesion molecule, CD 146, is expressed on ≈ 2% of normal circulating T cells, correlating with T cell activation, endothelial interactions and T helper type 17 ( T h17) effector functions. In this study, we have characterized CD 146 expression in circulating T cells from healthy controls and patients with stable, well‐controlled autoimmune connective tissue diseases ( CTD s). In vitro , anti‐ CD 3/anti‐ CD 28 stimulation induced CD 146 expression in both CD 4 and CD 8 T cells. In healthy controls and CTD patients, CD 146 was associated with expression of recent and chronic activation markers ( CD 25 + , OX ‐40 + , CD 69 + , CD 27 – ) and was confined to CD 45 RO + / RA – / CD 28 + populations within the CD 4 subset. Except for CD 69, these markers were not associated with CD 146 in the CD 8 subset. Surprisingly, most CTD patients exhibited no T cell hyperactivation ex vivo . In five of five patients with secondary S jögren's syndrome circulating T cells appeared activated despite therapy, and CD 146 up‐regulation, associated with activation markers, was observed both on CD 4 and CD 8 T cells. There was no association between CD 146 and putative pro‐atherogenic T cell subsets. In conclusion, the relationship of CD 146 expression to T cell activation differs between T cell subsets in healthy subjects and correlates with systemic hyperactivity, where present, in patients with CTD s, as exemplified by the patients with secondary S jögren's syndrome in this study.

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