Article Text

AB0526 B1 CD5+ lymphocytes in systemic lupus erythematosus patients: relation to disease activity
  1. SI Nasef1,
  2. HH Omar2,
  3. HH Omar3,
  4. MS Ghaly1
  1. 1Physical Medicine, Rheumatology and Rehabilitation
  2. 2Clinical Pathology
  3. 3Internal Medicine, Faculty of Medicine, Suez Canal University, Ismailia, Egypt


Background B cells are essential players in the pathogenesis of Systemic lupus erythematosus (SLE). Membrane CD5 elevates the threshold of B cell receptor mediated responses, and thus prevents the release of antibodies. So, misguided signalling through CD5 could lead to autoimmunity. Hence, CD5+ B cells were considered to play a paradoxical role in preventing rather than inducing autoimmunity. This challenging view differs from the old interpretation that elevated levels of B1 CD5+ cells in SLE patients represent a direct source of autoantibodies responsible for organ damage.

The clinical implications of this new concept for the role of B1 CD5+ cells in SLE have not been fully addressed yet and there is no consensus agreement about the proportions of B1 CD5+ cells in SLE patients. Moreover, the relation of B1 CD5+ cells to disease activity and organ damage is not sufficiently studied.

Objectives To assess the expression of B1 CD5+ cells in SLE patients and to evaluate their relationship with disease activity and organ damage.

Methods We recruited 100 SLE patients and 100 healthy control subjects. Based on SLE disease activity index (SLEDAI), patients were divided into two groups; active SLE (n=50) and inactive SLE (n=50). SLE was active when SLEDAI was ≥4. The expression of (CD5+CD20+) B1 cells was evaluated using flow cytometry. Lymphocytes were gated depending on both side and forward scatter. From the gated lymphocytes, B1a cells were identified double positive cells for CD20 and CD5. Percentage and absolute numbers of CD20+CD5+ (B1a cells) and their mean fluorescence intensity (MFI) were measured. The histogram of CD5 expression was used to assess its expression on CD20 cells (figure 1).

Laboratory work included CBC, ESR, CRP, Serum creatinine, Protein/creatinine ratio, Urine analysis, 24 hour protein collection in urine, Complement levels, (Anti-dsDNA) and (ANA).

Results Mean age of patients was 31.3±8.8 years. Females constituted 94% (n=94) of patients. Mean disease duration was 5.28±4.8 years. Mean SLEDAI was 10.28±5.16.

The proportions of (CD5+CD20+) B1 cells were significantly lower in SLE patients versus controls (5.9±4.4% vs 20.2±4%, p≤0.001). Similarly, the absolute numbers of (CD5+CD20+) B1 cells (cell/mm3) were significantly lower in SLE patients versus controls (100.2±103.4 vs 557.6±163.3, p≤0.001).

The expression of (CD5+CD20+) B1 cells was decreased in active SLE patients (4.5±3.8%) in comparison to inactive patients (7.3±4.7%) (p=0.027). B1 (CD5+CD20+) absolute cell number (cell/mm3) was significantly lower in active SLE patients (71.4±82.9) compared to inactive ones (129.0±115.1) (P=0.047). MFI of CD5+/CD20+ was significantly decreased in SLE patients compared to healthy control (146.9±109 vs 196±48, P=0.033). B1 cells (CD5+CD20+) correlated positively with C3 (r=0.322, p=0.022) and C4 (r=0.307, p=0.030). No correlation was found between (CD5+CD20+) B1 cells and disease duration, autoantibodies or any specific system or organ damage.

Conclusions Expression of B1 CD5+ cells was significantly decreased in SLE patients. Decreased B1 CD5+ cells expression was associated with higher disease activity. B1 CD5+ correlated positively with complement levels. These findings denote that CD5 expression on B cells may play a regulatory role in SLE pathogenesis and decrease occurrence of flares.

Disclosure of Interest None declared

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