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Further studies on the inhibition of lymphocytic choriomeningitis-induced glomerulonephritis by antiinterferon globulin. Circulating immune complexes and ultrastructural studies



Further studies on the inhibition of lymphocytic choriomeningitis-induced glomerulonephritis by antiinterferon globulin. Circulating immune complexes and ultrastructural studies



Laboratory Investigation; a Journal of Technical Methods and Pathology 43(1): 37-46



The development of glomerulonephritis that follows neonatal infection of mice with lymphocytic choriomeningitis (LCM) virus was markedly inhibited by treatment of the mice with anti-mouse interferon antibody. To understand further this phenomenon, 2 different types of investigations were performed. First circulating immune complexes were measured in neonatally LCM virus-infected mice, treated with sheep anti-interferon antibody, normal sheep serum or left untreated. Using 3 tests (virus-IgG complexes, [human lymphoblastoid] Raji cell assay and C1q binding assay) immune complexes were found in all 3 groups of mice infected with LCM virus. The levels were not significantly different in anti-interferon-treated mice, although the prevalence and severity of the glomerulonephritis were considerably decreased in this group until 80 days of age. Second, a sequential ultrastructural study of the early stages of the glomerulonephritis was performed in Swiss mice infected at birth with LCM virus and either left untreated or given injections of sheep anti-interferon antibody or normal sheep serum. By EM, abnormalities of the glomerular basement membrane similar to those induced by exogenous interferon could be detected in untreated mice infected at birth with LCM virus. The lesions characterized by thickening of the lamina rara interna containing areas of rarefaction were transient; maximal at day 16, they were barely detectable by day 58. At this time, electron-dense deposits could be detected in the mesangial spaces. At day 185 and 216, these deposits had increased in size but could also be found in control noninfected mice. The injection of anti-interferon antibody could completely inhibit the development of the glomerular basement membrane lesions. The protection provided by anti-interferon in the development of LCM virus-induced glomerulonephritis is not linked to a decreased amount of circulating immune complexes, but may be due to the inhibition of the local action of interferon on the glomerulus.

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Accession: 043171023

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PMID: 7392574


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