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Publication Detail
Abnormal CTLA-4 function in T cells from patients with systemic lupus erythematosus.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Jury EC, Flores-Borja F, Kalsi HS, Lazarus M, Isenberg DA, Mauri C, Ehrenstein MR
  • Publication date:
  • Pagination:
    569, 578
  • Journal:
    Eur J Immunol
  • Volume:
  • Issue:
  • Status:
  • Country:
  • Language:
  • Keywords:
    Antigens, CD, CD28 Antigens, CD3 Complex, CD4-Positive T-Lymphocytes, CTLA-4 Antigen, Flow Cytometry, Forkhead Transcription Factors, Humans, Lupus Erythematosus, Systemic, Lymphocyte Activation, Membrane Microdomains, Microscopy, Confocal, T-Lymphocytes
CTLA-4 is a critical gatekeeper of T-cell activation and immunological tolerance and has been implicated in patients with a variety of autoimmune diseases through genetic association. Since T cells from patients with the autoimmune disease systemic lupus erythematosus (SLE) display a characteristic hyperactive phenotype, we investigated the function of CTLA-4 in SLE. Our results reveal increased CTLA-4 expression in FOXP3(-) responder T cells from patients with SLE compared with other autoimmune rheumatic diseases and healthy controls. However, CTLA-4 was unable to regulate T-cell proliferation, lipid microdomain formation and phosphorylation of TCR-zeta following CD3/CD28 co-stimulation, in contrast to healthy T cells. Although lupus T cells responded in vitro to CD3/CD28 co-stimulation, there was no parallel increase in CTLA-4 expression, which would normally provide a break on T-cell proliferation. These defects were associated with exclusion of CTLA-4 from lipid microdomains providing an anatomical basis for its loss of function. Collectively our data identify CTLA-4 dysfunction as a potential cause for abnormal T-cell activation in patients with SLE, which could be targeted for therapy.
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