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Abstract Number: 687

Gammadelta T Cells and Their Intracellular Cytokine Profile in Peripheral Blood of Patients with Systemic Lupus Erythematosus

Lingyun Sun, Xia Li and Zhimin Lu, Department of Rheumatology and Immunology, the Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: T cells and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Human Etiology and Pathogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose: Gammadelta T cells represent a minor population of human peripheral blood T lymphocytes. As very rapid cytokine-producing cells, gammadelta T cells can regulate other ƒnlymphocytes activation and assist their local inflammatory function. Systemic lupus erythematosus (SLE) is a multi-organ damage autoimmune disease characterized by lymphocyte dysfunction and aberrant cytokine production. The aim was to detect gammadelta T cells numbers in the peripheral blood mononuclear cells (PBMCs) and analyze their intracellular cytokines profile (IFN-γ, IL-4, IL-10, IL-17, TGF-b).

Methods: Gammadelta T cells were detected in peripheral blood from 42 SLE patients and 20 normal controls by flow cytometry (FACS). Lupus disease activity was evaluated with a SLEDAI (SLE Disease Activity Index) score. Active SLE was defined as SLEDAI≥8. Annexin-V/PI double-staining FACS analysis was employed to observe the proportion of the apoptotic gammadelta T cells in 6 active SLE patients and 6 normal controls, respectively. The percentages of cytoplasmic cytokines including IFN-γ, IL-4, IL-10, IL-17 and TGF-b were examined in 20 SLE patients and 10 normal controls by FACS analysis.

Results: The percentages of gammadelta T cells were remarkably down-regulated in active SLE patients (2.96±1.84%, n=30) compared with that of inactive (5.31±3.05%, n=12) and normal controls (6.83±2.85 %, n=10, both p<0.01). The absolute number of gammadelta T cells decreased significantly in active SLE patients (1.72±1.58×107/L, n=30) than that in inactive SLE (5.27±3.60×107/L, n=12, p<0.01), both lower than in normal controls (10.07±4.99 ×107/L, n=10, both p<0.01). There was increased gammadelta T cells apoptosis (17.03±8.71%, n=6) in SLE patients than in normal controls (6.67±1.18%, n=6, p<0.05). The positive rate of gammadelta T intracellular IFN-γ, IL-4, IL-10 and TGF-bƒn production in 20 SLE patients were 33.19±20.20 %, 1.04±0.93 %, 1.91±0.98 % and 2.20±1.97 %, significantly higher than that of 10 normal controls (IFN-γ:ƒn5.87±4.63%, IL-4: 0.30±0.34%, IL-10: 0.18±0.31%, TGF-bƒª0.21±0.22%, all p < 0.01). While there were no differences in the percentages of IL-17-positive gammadelta T cells betweenƒn SLE patients (0.14±0.24%, n=20) and normal controls (0.18±0.31%, n=10).

Conclusion: Gammadelta T cells are down-regulated in SLE partly due to excessive apoptosis. Gammadelta T cells secret both pro- and anti-inflammatory cytokines in SLE microenvironment, suggesting these cells participate in both the regulation and the propagation of lupus.


Disclosure:

L. Sun,
None;

X. Li,
None;

Z. Lu,
None.

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