Abnormality of Oct‐1 DNA binding in T cells from Sjögren's syndrome patients

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Abstract
Primary Sjögren's syndrome (SS) is an autoimmune rheumatic disease characterized by T cell hypoactivity. To understand the diminished T cell response to activation signals, we measured nucleoprotein DNA‐binding activities regulating gene expression during T cell activation using the electrophoretic mobility shift assay. Peripheral blood lymphocytes from 9/19 SS patients were found to be defective in their ability to bind an octomer sequence (Oct‐1). This Oct‐1‐binding phenotype remained stable in culture for up to 3 days prior to activation. This abnormality was not seen in resting T cells nor T cells from patients with systemic lupus erythematosus, rheumatoid arthritis (RA), or SS accompanied by RA. The SS Oct‐1 DNA‐binding abnormality correlated significantly with an inability of cells to exit the G0/G1 cell cycle phase when stimulated in vitro. Importantly, nucleoprotein extracts showing decreased DNA‐binding activity had normal amounts of Oct‐1 proteins as determined by immunoprecipitation, implying a functional defect in the Oct‐1 protein. Moreover, defective DNA binding was corrected by treatment with acid phosphatase.