Abnormality of Oct-1 DNA binding in T cells from Sjögren's syndrome patients
| Autor: | Toru Nakabayashi, Howard Dang, Norman Talal, Juan-Manuel Anaya, Eliezer Flescher, Noriyoshi Ogawa, Norma Vela-Roch, Agustin Escalante |
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| Rok vydání: | 1996 |
| Předmět: |
Adult
Male medicine.medical_specialty Immunoprecipitation T-Lymphocytes T cell Molecular Sequence Data Immunology Biology Internal medicine Gene expression medicine Humans Immunology and Allergy Electrophoretic mobility shift assay RNA Messenger Phosphorylation Aged Homeodomain Proteins Base Sequence DNA T lymphocyte Middle Aged medicine.disease In vitro DNA-Binding Proteins Sjogren's Syndrome medicine.anatomical_structure Endocrinology Rheumatoid arthritis Interleukin-2 Female Carrier Proteins Host Cell Factor C1 G1 phase Octamer Transcription Factor-1 Transcription Factors |
| Zdroj: | European Journal of Immunology. 26:2006-2011 |
| ISSN: | 1521-4141 0014-2980 |
| DOI: | 10.1002/eji.1830260906 |
| Popis: | 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 october 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 Gzero/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. |
| Databáze: | OpenAIRE |
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