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Hematoxylin-stained bodies and tissue "LE cells" have been identified for the first time in a skeletal muscle biopsy from a 46-year-old white female with clinical and laboratory evidence of systemic lupus erythematosus. The specificity and limited usefulness of hematoxylin bodies are discussed.
Lewis phenotyping of 487 blood samples from Chinese newborn infants and young children, revealed that 50% of cord cells were Le(a-b+) and 50% Le(a-b-). The weak Leb antigen of Le(a-b+) cord cells is most likely produced by the newborn infant rather than of maternal origin and it appears that these infants eventually develop by way of an intermediate Le(a+b+) stage into the adult Le(a-b+) phenotype. Most infants with Le(a-b-) cord cells, but not all, appear to develop through a transitional Le(a+b-) stage, into Le (a+b+) by about 1 month of age, most likely continuing as such into adulthood. This development of Le(a-b-) cord cells into the adult Le(a+b+) phenotype is postulated to be the result of the weak secretor gene Se omega. Those infants with Le(a-b-) cord cells that do not convert to Le(a+b+) during the first month of life, most likely remain as such into adulthood. The blood of 120 adult voluntary blood donors, used as controls, reconfirmed adult Chinese phenotypic frequencies of approximately 70% Le(a-b+), 22% Le(a+b+) and 8% Le(a-b-).
In the course of a prospective study of 165 patients with SLE a subgroup of eight patients with active SLE yet with persistently negative tests for ANF and LE cells was identified. These patients were characterized by a photosensitive skin rash with a negative lupus band test, a high incidence of arthritis, mild form of renal disease, and a positive family history for connective tissue disease. Antibodies to DNA and cytoplasmic antigens were detected in a few.
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Apoptotic cell death, phagocytic uptake, and their interplay may induce/trigger autoantibody production and autoimmunity. Herein the role of immunoglobulin G (IgG) anti-dsDNA autoantibodies in nucleo-phagocytosis by polymorpho-nuclear cells (PMN) has been analyzed. Necrotaxis, phagocytosis and PMN with engulfed nuclei can be imaged by vital microscopy. Vital microscopy revealed dead neutrophils with persistence of nuclei or ingested nuclei in 8/10 patients with lupus erythematosus (LE) and in 4/20 healthy controls (P < 0.0006). The phagocytic clearance of dead cells/nuclei did not correspond to any of the analyzed apoptosis markers (annexin V, CD95, and active caspase 3). IgG staining of isolated PBMC nuclei as detected by flow cytometry was significantly higher in parallel to NUC+ (P < 0.02). In vitro phagocytosis of substrates pre-treated with anti-dsDNA containing serum induced an increased phagocytic capacity as compared to normal serum. These data suggest that anti-dsDNA antibodies seem to inhibit enzymatic cleavage of nuclei from damaged cells, and improve their phagocytic uptake by PMN, which finally results in LE cell formation.
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1. The effects of antinuclear antibodies on nuclear material can be observed directly in free leucocyte nuclei in the supravital preparation according to Engel. 2. The antinuclear antibodies prevent the lysis of free nuclei, they obstruct the normal degeneration of nuclei. 3. The nuclear blockade is recognizable in the dark-clodded, rigid nuclei which remain small. These blocked nuclei are the visible expression of a development of complexes between chromatin and antinuclear antibodies. 4. It is supposed that the protective effect of antinuclear antibodies consists of the obstruction of the DNases and histon-proteases bound to chromatin. 5. The effects of antinuclear antibodies is in agreement with the structure of the nucleosomes of chromatin. 6. The nuclear blockade caused a persistence of antigenic material, which can create an increase of antibody production. This means that in vivo the antinuclear blockade is an effect which sustains illness.
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