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Publication Detail
Impaired C3b/iC3b deposition on Streptococcus pneumoniae in serum from patients with systemic lupus erythematosus.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Goldblatt F, Yuste J, Isenberg DA, Rahman A, Brown J
  • Publication date:
  • Pagination:
    1498, 1501
  • Journal:
    Rheumatology (Oxford)
  • Volume:
  • Issue:
  • Status:
  • Country:
  • PII:
  • Language:
  • Keywords:
    Adult, Aged, Complement C3b, Complement Pathway, Classical, Humans, Immune Tolerance, Lupus Erythematosus, Systemic, Middle Aged, Opportunistic Infections, Phagocytosis, Pneumococcal Infections, Streptococcus pneumoniae
OBJECTIVE: To determine whether opsonization of Streptococcus pneumoniae with C3b/iC3b is impaired in serum from patients with SLE. METHODS: The ability of serum samples from 30 patients with SLE, 20 with non-SLE rheumatic diseases (RA, PsA, AS, SS) and 20 healthy controls to opsonize S. pneumoniae (strains D39 and Io11697) with C3b/iC3b was assessed using a standardized FACS technique and a FACSCalibur flow cytometer. Results were compared among the three groups using analysis of variance, followed by pairwise comparisons among groups using the Mann-Whitney U-test. RESULTS: The proportion of bacteria positive for C3b/iC3b was significantly lower in serum from patients with SLE (strain D39: 60.3% +/- s.e.m. 2.87, strain Io11697: 55.3% +/- 3.8) compared with healthy controls (strain D39: 70.6% +/- 2.0, P = 0.01; strain Io11697: 67.8% +/- 2.6; P = 0.05) and non-SLE rheumatic controls (strain D39: 69.8% +/- 3.1; P = 0.03). For the patients with SLE, there was no association between C3b/iC3b deposition and serum complement levels or measurable classical pathway activity. C3b/iC3b deposition on S. pneumoniae was significantly lower in serum from SLE patients with a past history of pneumonia (n = 3) compared with those without (n = 27; P = 0.03). CONCLUSIONS: Opsonization of S. pneumoniae with C3b/iC3b was significantly reduced in serum from patients with SLE compared with non-SLE rheumatic disease and healthy controls. Failure to appropriately activate the immune system via complement may contribute to the increased susceptibility of SLE subjects to infections, and may correlate with a risk of pneumonia in a subgroup of SLE patients.
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