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      Pathogenesis of lipoid nephrosis: a disorder of T-cell function.

      Lancet

      Viral Interference, immunology, Thymus Gland, T-Lymphocytes, pharmacology, Steroids, Remission, Spontaneous, Pneumococcal Infections, complications, Phagocyte Bactericidal Dysfunction, etiology, Nephrosis, Lipoid, Measles virus, Male, cytology, Kidney Glomerulus, biosynthesis, Interferons, Immunologic Deficiency Syndromes, Immunity, Cellular, Humans, Hodgkin Disease, Female, Cyclophosphamide, Cell Membrane Permeability, Basement Membrane

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          Abstract

          Clinical observations suggest that lipoid nephrosis is produced by a systemic abnormality of T-cell function resulting in the secretion of a circulating chemical mediator toxic to an immunologically innocent glomerular basement membrane. The lack of evidence of a humoral antibody response, remission induced by measles which modifies cell-mediated immunity, the therapeutic benefits of steroids and cyclophosphamide which also abate cell-mediated responses, and the occurrence of this syndrome in Hodgkin's disease support this hypothesis. The susceptibility of untreated patients to pneumococcal infections may be of primary or secondary pathogenetic importance. Taken together, the data suggest that this syndrome is a clinical expression of a self-limited primary immune-deficiency disease.

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          4140273

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