Transplacental passage of antinuclear antibody. Study in infants of mothers with systemic lupus erythematosus

Beck, J. Swanson

doi:10.1001/archderm.93.6.656

Cited by 28 publications

(7 citation statements)

References 32 publications

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“…This is consistent with observations in SLE where it has been shown that antinuclear antibodies by themselves were not pathogenic in vivo (33,34) or cytotoxic to tissue culture cells in vitro (35,36). The experimental observations reported here point to the need, however, for vigilance in the care of patients with SLE who have circulating antibodies to DNA, since small amounts and brief episodes of immune complex formation in the circulation might occur unnoticed.…”

Section: Methodssupporting

confidence: 91%

Experimental Renal Disease Induced by DNA—Anti-DNA Immune Complexes

Natali¹,

Tan²

1972

J. Clin. Invest.

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A B S T R A C T Rabbits immunized with ultraviolet-irradiated DNA (UV-DNA) produced high titers of serum antibody. This experimental model was studied to determine if injection of antigen (UV-DNA) intravenously into immunized animals would induce glomerulonephritis and proteinuria. Proteinuria was observed several days after the start of daily intravenous injections into immunized animals and was sustained as long as injections were continued, but fell to normal values after stopping antigen administration. The kidneys showed glomerulitis sometimes associated with focal proliferative lesions, and immunofluorescence showed rabbit Ig and C3 in glomeruli. By electron microscopy, electron-dense subendothelial deposits were seen. Sucrose density gradient analyses of sera immediately after antigen injections suggested the presence of immune complexes of DNA and antibody since both heavy sedimenting and 7S Ig were detected. After digestion with deoxyribonuclease rabbit Ig could be found only in the 7S sedimenting fractions. Intravenous injection of UV-DNA into normal, nonimmune animals did not produce heavy sedimenting Ig or abnormal sedimentation patterns. These studies with an experimental model might provide insight into pathogenetic mechanisms operating in systemic lupus erythematosus where the importance of DNA-anti-DNA immune complexes have been documented. The studies suggested that gradual accumulation of DNA immune complexes in glomeruli might be one mechanism causing renal functional abnormalities.

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Section: Methodssupporting

confidence: 91%

Experimental Renal Disease Induced by DNA—Anti-DNA Immune Complexes

Natali¹,

Tan²

1972

J. Clin. Invest.

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“…While autoantibodies may be involved in the development of some of the lesions (Koffler, Schur, and Kunkel, 1967), they cannot by themselves be the prime cause of the disease (Beck, Oakley, and Rowell, 1966). Interest has recently centred once more on infective agents with reports of virus-like particles in many of the tissues of SLE (Norton, 1969;Bariety, Amor, Kahan, Balafrej, Callard, and Delbarre, 1971;Garancis, Komorowski, Bernhard, and Straumfjord, 1971) coming as a sequel to earlier reports of the isolation of mycoplasmas (Bartholomew, 1965;Jansson, Vainio, and Tuuri, 1971).…”

mentioning

confidence: 99%

Leucocyte migration-inhibition in systemic lupus erythematosus.

Hughes¹,

Holt²,

Rowell³

1974

Annals of the Rheumatic Diseases

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“…However, in 1966, Beck et a1 (31) reported the transplacental passage of 7 .OS gamma globulin, the antinuclear antibody, from 3 mothers with SLE. The infants were studied serologically, but failed to manifest any disease associated with LE.…”

Section: Discussionmentioning

confidence: 99%

Neonatal lupus erythematosus occurring in one fraternal twin. Serologic and immunogenetic studies

Callen

Fowler

Kulick

et al. 1985

Arthritis & Rheumatism

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Neonatal lupus erythematosus (LE) is a syndrome that is manifested by LE skin lesions and/or congenital heart block, occurring in infants at, or shortly after, birth. The syndrome is believed to be caused by transplacental passage of an IgG antibody, usually the anti‐Ro (SS‐A) antibody, from the mother to the infant. Although the mother may have a connective tissue disease or may be healthy, the common characteristic is the presence of maternal circulating anti‐Ro antibody. It has been believed that the HLA determinants demonstrated in children who have neonatal LE were not a factor in the expression of the syndrome. We report the occurrence of neonatal LE, manifested by photosensitivity and discoid LE skin lesions, in one fraternal twin. HLA studies of this affected twin demonstrated the presence of DR3. Anti‐Ro antibody was present in the mother, but was not present in either child at 4 months post‐delivery. HLA determinants may be involved in the expression of disease in neonates who have been exposed to the anti‐Ro antibody. Furthermore, the presence of circulating antibodies in the unaffected twin causes us to question the assumption that the anti‐Ro antibody is the causative factor for the occurrence of tissue injury in children with neonatal LE.

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Transplacental passage of antinuclear antibody. Study in infants of mothers with systemic lupus erythematosus

Cited by 28 publications

References 32 publications

Experimental Renal Disease Induced by DNA—Anti-DNA Immune Complexes

Experimental Renal Disease Induced by DNA—Anti-DNA Immune Complexes

Leucocyte migration-inhibition in systemic lupus erythematosus.

Neonatal lupus erythematosus occurring in one fraternal twin. Serologic and immunogenetic studies

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