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N F Rothfield

Publications and source records attributed to N F Rothfield.

At least 91 records · Page 5Linked to original sources
PubMed1967

The relation of immunoglobulin class, pattern of anti-nuclear antibody, and complement-fixing antibodies to DNA in sera from patients with systemic lupus erythematosus.

Sera from 55 patients with systemic lupus erythematosus were studied to clarify the significance of the patterns of nuclear fluorescence observed. The sera in which the IgG fraction produced a peripheral pattern of nuclear fluorescence were found to contain complement-fixing antibodies to native DNA and to DNA-histone complexes. This correlation did not exist when complement-fixing activity was compared to the IgM nuclear patterns. Sera which contained only complement-fixing antibodies to denatured DNA and which did not react with native DNA or nucleoprotein did not produce the peripheral pattern of nuclear fluorescence. The data suggest that single strands of DNA were not the reactive groups in the nucleus responsible for the peripheral pattern. The results support the conclusion that DNA within a DNA-protein complex may be the nuclear antigen responsible for the peripheral pattern of nuclear fluorescence. Analysis of the clinical data revealed that a close correlation existed between the presence of IgG peripheral pattern, complement-fixing antibodies to DNA and histone-DNA complexes, and clinical manifestation of active disease.

Antibodies↗
PubMedDate not supplied

Family study of systemic lupus erythematosus: analysis of the clinical history, skin immunofluorescence, and serologic parameters.

The clinical history, deposition of IgG, IgM, IgA, C3, C4 and properdin at the dermal-epidermal junction (DEJ) of clinically normal skin, serum ANA, DNA-binding, C3, C4, Factor B, and properdin were compared in 27 systemic lupus erythematosus (SLE) probands, 21 first-degree household contact relatives (FDHCR), 19 first-degree nonhousehold contact relatives (FDNHCR), 15 spouses, 26 controls, and 16 chronic discoid lungs lupus erythematosus patients. Female consanguineous relatives of SLE patients had a higher incidence of rheumatic symptoms than male relatives (P less than 0.01). Female FDHCR and male spouses had a higher incidence of protein deposition at the DEJ than sex-matched controls (P = 0.026 and 0.0028). The incidence of protein deposition at the DEJ in FDNHCR did not differ from sex-matched controls. ANA titers of the consanguineous relatives were significantly higher than those of the spouses or sex-matched controls irrespective of household contact with their proband. The observation of protein deposition at the DEJ in normal appearing skin of FDHCR and spouses suggests the importance of environmental factors, whereas the elevations of ANA titers in consanguineous relatives suggests the importance of genetic factors in the pathogenesis of SLE.

Adolescent↗
PubMedDate not supplied

Prostaglandin E1 treatment of NZB/NZW F1 hybrid mice. II. Prevention of glomerulonephritis.

The F1 hybrid of New Zealand black and New Zealand white mice--the NZB/NZW mouse--spontaneously develops a disease similar to human systemic lupus erythematous, characterized by impaired cell-mediated and enhanced humoral immune responses, development of antibodies to nuclear antigens, and immune complex glomerulonephritis. Because there is experimental evidence that prostaglandin E1 (PGE1) can enhance T-cell function and cell-mediated responses and suppress B-cell activity, NZB/NZW mice were treated with 200 microgram PGE1 subcutaneously once or twice daily from 6 weeks of age. PGE1 treatment of female and male mice prevents giomerular deposition of immunoglobulins and complement (monitored by immunofluorescence), and development of the proliferative glomerulonephritis (determined by light and electron microscopy) characteristic of untreated NZB/NZW mice. After 1 year of treatment, 18 of 19 female mice survived, whereas only 2 of 19 untreated control mice were alive. Male mice treated with 200 microgram PGE1 daily were also protected: 9 of 11 versus 2 of 9 untreated mice were alive at 65 weeks. PGE1 treatment did not prevent development of antibodies to nuclear material in any of the treated groups.

Animals↗