Increased expression of the B-cell-regulatory molecule CD72 in primary Sjögren's syndrome.
To determine whether there is an intrinsic abnormality of B-cell signaling in primary Sjögren's syndrome (pSS), the expression of B-cell coreceptors was determined in patients with primary Sjögren's syndrome and healthy and disease controls. Peripheral blood mononuclear cells were labeled with monoclonal antibodies to CD21, CD22, or CD72, and then the pan B-cell marker CD19. The expression of these coreceptors on the total CD19(+) population was determined. There was a significant increased expression of CD72 on the B cells of pSS patients (MFI, 215 +/- 6) compared to normal controls (MFI, 141 +/- 6). The increased CD72 expression was disease specific for pSS, as it was not observed in systemic lupus erythematosus or rheumatoid arthritis. The effect of B-cell stimulation on coreceptor expression was determined by culturing cells with B-lymphocyte-activating factor (BAFF) and/or pokeweed mitogen (PWM) or without either. Following culture, CD72 expression was decreased in both pSS and normal controls, regardless of the presence of BAFF or PWM. The upregulation of CD72 in pSS might be a compensatory response to increased B-cell receptor stimulation or a primary abnormality leading to uncontrolled B-cell activation.[1]References
- Increased expression of the B-cell-regulatory molecule CD72 in primary Sjögren's syndrome. Smith, A.J., Gordon, T.P., Macardle, P.J. Tissue Antigens (2004) [Pubmed]
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