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Publication Detail
Characterization of CD3+ CD4- CD8- (double negative) T cells in patients with systemic lupus erythematosus: activation markers
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Anand A, Dean GS, Quereshi K, Isenberg DA, Lydyard PM
  • Publication date:
    2002
  • Pagination:
    493, 500
  • Journal:
    Lupus
  • Volume:
    11
  • Issue:
    8
  • Print ISSN:
    0961-2033
  • Keywords:
    ACTIVATION, activation markers, activity, adolescent, adult, Aged, analysis, anti-DNA, antibodies, Antibody, ANTIGEN, Antigens, Antigens, CD, Antigens, CD28, Antigens, CD3, Antigens, CD4, Antigens, CD45, Antigens, CD8, Antigens, Differentiation, Antigens, Differentiation, T-Lymphocyte, Antigens, Surface, Arthritis, As, Autoantibodies, B CELL, B-cell, Biological Markers, CD28, CD4, CD45, CD45RA, CD8, cell, CELL-SURFACE, CELLS, characterization, chemistry, control, Correlation, diagnosis, differentiation, disease, expression, Female, HEALTHY, HLA-DR, HLA-DR Antigens, HYPERACTIVITY, IM, immunology, INCREASE, LA, LEVEL, Lupus, Lupus Erythematosus, Systemic, Lymphocyte Activation, Magnetic, Male, MARKER, Markers, Middle Age, Molecule, PARAMETER, PARAMETERS, Patient, patients, PERCENTAGE, Phenotype, population, Rheumatoid arthritis, RHEUMATOID-ARTHRITIS, separation, serum, SEVERITY, SLE, Staining, SURFACE, SYSTEMIC, SYSTEMIC LUPUS ERYTHEMATOSUS, SYSTEMIC-LUPUS-ERYTHEMATOSUS, T cell, T CELLS, T lymphocyte, T-CELL, T-CELLS, T-Lymphocytes, TCR
  • Notes:
    UI - 22208411 DA - 20020910 IS - 0961-2033 LA - eng PT - Journal Article RN - 0 (Antigens, CD) RN - 0 (Antigens, CD28) RN - 0 (Antigens, CD3) RN - 0 (Antigens, CD4) RN - 0 (Antigens, CD45) RN - 0 (Antigens, CD8) RN - 0 (Antigens, Differentiation) RN - 0 (Antigens, Differentiation, T-Lymphocyte) RN - 0 (Antigens, Surface) RN - 0 (Biological Markers) RN - 0 (CD69 antigen) RN - 0 (CTLA-4) RN - 0 (HLA-DR Antigens) SB - IM
Abstract
Systemic lupus erythematosus (SLE) is characterized by B cell hyperactivity and the production of autoantibodies, some of which (antibodies to dsDNA) are thought to be pathogenic. T helper cells drive the production of autoantibodies and the aim of this study is to characterize phenotypically a subpopulation of T cells (the CD3+ CD4- CD8-, double negative (DN) T cells) previously identified as helping to enhance anti-DNA antibodies in patients with SLE. Data were obtained using FACS staining of DN T cells that had been purified from PBMCs by magnetic bead separation. The percentage of TCR alphabeta+ DN T cells was found to be significantly higher in patients with SLE as compared with controls (P = 0.02), although there was no significant increase in total percentage of DN T cells, which includes TCR gammadelta+ cells. Activation markers HLA-DR and CD69, the costimulatory molecule CD28 and CTLA-4 were all expressed on the surface of a higher percentage of DN T cells in patients with SLE than in patients with rheumatoid arthritis (RA) or healthy controls (HC). More DN T cells from patients with SLE were of CD45RA phenotype than was found in controls, while CD45RO-expressing cells were reduced. In addition, DN T cells from patients with SLE expressed significantly higher levels of HLA-DR (P = 0.006), CD28 (P = 0.05), CTLA4 (P = 0.03) and CD45RA (P = 0.05) on the cell surface than those from the CD4/8 population. Correlation of expression of the markers measured with various parameters of disease activity and severity showed that high levels of HLA-DR expression correlated with high circulating serum C3 (> 0.9 IU/ml), indicating that an activated phenotype is consistent with severe disease
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