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There is evidence in favor of apoptosis dysfunction being involved in the pathogenesis of SLE. Since mice deficient in the nucleosome-binding protein: serum amyloid P component (SAP) develop antinuclear immunity and nephritis it is possible that impaired clearance of nuclear material from apoptotic cells is the key defect. We therefore developed a solid-phase assay for the binding of SAP to nucleosomes and investigated the nucleosome binding characteristics of SAP from 20 different SLE patients as compared with normal donors. We could not demonstrate any significant differences between the groups and therefore the functions of other pentraxins (such as C-reactive protein) or DNA binding molecules (such as C1q) will be examined in future studies.