Quantitative T cell subsets profile in peripheral blood from patients with idiopathic inflammatory myopathies: tilting the balance towards proinflammatory and pro‐apoptotic subsets
Author(s) -
EspinosaOrtega F.,
GómezMartin D.,
SantanaDe Anda K.,
RomoTena J.,
VillaseñorOvies P.,
AlcocerVarela J.
Publication year - 2015
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.12475
Subject(s) - foxp3 , cxcr3 , immunology , t cell , cd8 , il 2 receptor , flow cytometry , cd28 , rar related orphan receptor gamma , cxcr5 , peripheral blood mononuclear cell , proinflammatory cytokine , c c chemokine receptor type 6 , medicine , ccr4 , biology , inflammation , immune system , chemokine , biochemistry , chemokine receptor , in vitro
Summary The role of T cells in idiopathic inflammatory myopathies ( IIM ) is not yet clear. Some alterations in certain subsets have been reported in inflamed muscle cells. However, a broad quantitative assessment of peripheral T cell subsets has not been evaluated. The aim of this study was to address the quantitative profile of potential pathogenic T cell subsets, namely follicular helper T cells ( T fh), T helper type 17 ( T h17), CD 28 null and regulatory T cells ( T regs ) in peripheral blood from IIM patients. Thirty IIM patients and 30 age‐ and gender‐matched healthy donors were included. Peripheral blood mononuclear cells were isolated. T cell subsets were evaluated by flow cytometry, as follows: T fh ( CD 4 + CXCR 5 + ) and its subsets T fh1 ( CXCR 3 + CCR 6 − ), T fh2 ( CXCR 3 − CCR 6 − ), T fh17 ( CXCR 3 − CCR 6 + ), T h17 ( CD 4 + IL 17 A + ), CD 28 null ( CD 4 + CD 28 − CD 244 + ) and T regs ( CD 4 + CD 25 high forkhead box protein 3 (FoxP 3 + ); CD 8 + CD 25 high FoxP 3 + ). Percentage, absolute numbers and mean fluorescence intensity were analysed. We found increased numbers of total T fh cells (28 ± 8·16 versus 6·64 ± 1·29, P = 0·031) in IIM patients when compared to healthy controls. Moreover, this increment was dependent upon T fh2 and T fh17 ( T fh2:9·49 ± 2·19 versus 1·66 ± 0·46, P = 0·005; T fh17 9·48 ± 2·83 versus 1·18 ± 0·21, P = 0·014). Also, IIM patients showed higher numbers of T h17 cells (30·25 ± 6·49 versus 13·46 ± 2·95, P = 0·031) as well as decreased number of T regs (5·98 ± 1·61 versus 30·82 ± 8·38, P = 0·009). We also found an expansion of CD 28 null cells (162·88 ± 32·29 versus 64 ± 17·35, P = 0·015). Our data suggest that IIM patients are characterized by an expansion of peripheral proinflammatory T cells, such as T fh and T h17, as well as pro‐apoptotic CD 28 null cells and a deficiency of suppressor populations of T regs ( CD 4 + and CD 8 + ).
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