title: Assay of T- and NK-cell subsets and the expression of NKG2A and NKG2D in patients with new-onset systemic lupus erythematosus.
abstract: 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.
authors.affiliation: Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, 230032, People's Republic of China.
authors.forename: Wen-Xian
authors.initials: WX
authors.lastname: Li
authors.forename: Hai-Feng
authors.initials: HF
authors.lastname: Pan
authors.forename: Jian-Li
authors.initials: JL
authors.lastname: Hu
authors.forename: Chang-Zhong
authors.initials: CZ
authors.lastname: Wang
authors.forename: Ning
authors.initials: N
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Xiang-Pei
authors.initials: XP
authors.lastname: Li
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Xu
authors.forename: Dong-Qing
authors.initials: DQ
authors.lastname: Ye
mesh_terms: 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
chemical_list: 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