Assay of T- and NK-cell subsets and the expression of NKG2A and NKG2D in patients with new-onset systemic lupus erythematosus.
This study aims to explore the percentage of T-cell and NK-cell subsets, the expression of NKG2A and NKG2D on CD3+ T cells and CD3-CD56+ NK cells on the total lymphocytes in new-onset systemic lupus erythematosus (SLE) patients, and explore clinical significance of these cell subsets. Thirty-two SLE patients and 32 normal controls were enrolled. Flow cytometry was used to count T- and NK-cell subsets and to detect the expression of NKG2A and NKG2D on CD3+ T cells and CD3-CD56+ NK cells in patients with new-onset SLE. Results show that CD4+ T (t = 2.04, P < 0.05), CD4+/CD8+ T cell (t = 2.66, P < 0.05), CD4+ CD25+ T (t = 2.48, P < 0.05), CD3+CD56+ natural killer T (NKT) (t = 40.05, P < 0.01), CD3-CD56+CD16+ NK-cell subsets (t = 3.50, P < 0.01) were significantly decreased, CD8+ T-cell subsets was significantly increased in patients with new-onset SLE (t = 3.80, P < 0.01), as compared with healthy controls. CD8+ T-cell subset was significantly increased in patients with vasculitis (t = 2.47, P < 0.05), and CD3-CD56+CD16+ NK was increased in patients with arthritis (t = 3.21, P < 0.01). However, no statistically significant correlation was found among different PBMC subsets and SLEDAI activity scores. Patients with SLE had a lower expression of NKG2A (U = 2.42, P < 0.05) as well as NKG2A/NKG2D ratio (t = 2.61, P < 0.05) and a higher expression of NKG2D (t = 2.21, P < 0.05) on CD3+ T cells, compared with normal controls. However, they had a higher expression of NKG2A (t = 2.59, P < 0.05) as well as NKG2A/NKG2D ratio (t = 49.45, P < 0.01) and a lower expression of NKG2D (t = 3.05, P < 0.01) on CD3-CD56+ NK cells. Taken together, the findings indicate the decreased CD4+ T-cell, CD4+/CD8+ T-cell, CD4+CD25+ T-cell, CD3+CD56+ NKT-, and CD3-CD56+CD16+ NK-cell subsets, increased CD8+ T-cell subsets as well as the abnormal expression of NKG2A and NKG2D on CD3+ T and CD3-CD56 + NK cells may play a role in the etiology of SLE.
Li
Wen-Xian
WX
Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, 230032, People's Republic of China.
Pan
Hai-Feng
HF
Hu
Jian-Li
JL
Wang
Chang-Zhong
CZ
Zhang
Ning
N
Li
Jing
J
Li
Xiang-Pei
XP
Xu
Jian-Hua
JH
Ye
Dong-Qing
DQ
D000293:Adolescent; D000328:Adult; D017668:Age of Onset; D017252:CD3 Complex / Q000378:metabolism; D019002:CD56 Antigen / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007694:Killer Cells, Natural / Q000378:metabolism / Q000473:pathology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000473:pathology*; D018655:Lymphocyte Count; D008297:Male; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000378:metabolism*; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000378:metabolism / Q000473:pathology*; D055815:Young Adult
D017252:CD3 Complex; D019002:CD56 Antigen; C527054:KLRC1 protein, human; C527085:KLRK1 protein, human; D055654:NK Cell Lectin-Like Receptor Subfamily C; D055655:NK Cell Lectin-Like Receptor Subfamily K