Mononuclear cells from peripheral blood of normal humans, unselected spleen cells from patients with Hodgkin's disease, and selected T and non-T lymphoid cells from normal peripheral blood and from the spleens of Hodgkin's disease patients were examined for de novo synthesis and secretion of ferritin. After precipitation of labeled lysates and supernatants from unseparated and selected T cells with antiserum to human liver ferritin, two bands were visible on sodium dodecyl sulfate-polyacrylimide gel analysis. The two bands were detected in molecular weight regions 19,000 and 21,000, which are thought to represent the L and H subunits of the ferritin molecule, respectively. The slower band (subunit H) was more radioactive than the faster band (subunit L). The H subunit is found in greater amounts in the serum of some tumor patients, but its cellular origin has not been established. The present findings indicate that cells of the immune system contribute to the synthesis and secretion of a ferritin molecule with a high proportion of H subunits.
To investigate the incidence, the specificity and clinical significance of positivity for serum anti-neutrophil cytoplasmic antibody (ANCA) in 31 patients with systemic lupus erythematosus (SLE), the indirect immunofluorescence (IIF) technique and enzyme-linked immunosorbent assay (ELISA) were used to measure ANCA. Purified myeloperoxidase (MPO), lactoferrin (LF), cathepsin-G (CTG) and elastase (HLE) served as ANCA antigens for ELISA. Thirteen (42%) of the 31 SLE patients showed positivity for perinuclear, but not cytoplasmic, ANCA by IIF. Five of 31 sera were positive for MPO, 10 for LF, 1 for CTG and 0 for HLE by ELISA. Patients positive for ANCA had a higher score of SLE disease activity index (SLEDAI) than those without ANCA. There was no correlation between ANCA positivity, clinical manifestations, or organic involvement. While the ANCA in patients with SLE reflected disease activity, it was unrelated to organic involvement.
A 77-year-old Japanese womanwith massive painless ascites caused by chronic lupus peritonitis is reported. Peritoneal effusion had been resistant to the administration of steroids during the whole treatment period. It was characteristic that the titers of anti-DNA antibodies and the level of immunecomplex were elevated in the peritoneal fluid with suppressed levels of complements in ascites, although serum immunological markers reflecting the activity of SLE presented improvement after initiation of the treatment. Fifteen patients with chronic lupus peritonitis were reported previously. Wereviewed the literature and suggest that chronic lupus peritonitis at elderly onset may demonstrate a poor response to the glucocorticoid therapy because of persistent inflammation in the peritoneum and the presence of impaired vascular circulation in addition to immunological mechanisms.
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