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Results for “Phagocyte Bactericidal Dysfunction”

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PubMed1974

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

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.

Basement Membrane↗
PubMed1975

Phagocytosis in patients and carriers of chronic granulomatous disease.

The phagocytic capacity of leucocytes from four patients and two carriers of chronic granulomatous disease (C.G.D.) was compared to that of normal leucocytes. Leucocytes from C.G.D. patients phagocytised more Staphylococcus aureus than did normal leucocytes after 5, 10, and 20 minutes of incubation. Phagocytosis by leucocytes from two carriers of C.G.D. was intermediate between that in the patients and in controls. In contrast, phagocytosis of Streptococcus faecalis, an organism readily killed by C.G.D. leucocytes, was similar for control and C.G.D. leucocytes. Enhanced phagocytosis may represent an attempt by leucocytes to compensate for a bactericidal abnormality. In addition, these observations may partly explain why carriers of C.G.D. are not more susceptible to infection despite abnormal leucocyte function. Detection of carriers using the described assay of phagocytosis appears relatively simple compared to previously described methods.

Blood Bactericidal Activity↗