Interferon Gamma-1b

@article{Todd2012InterferonG,
  title={Interferon Gamma-1b},
  author={Patricia A. Todd and Karen L. Goa},
  journal={Drugs},
  year={2012},
  volume={43},
  pages={111-122}
}
SummarySynopsisChronic granulomatous disease is a group of rare x-linked or autosomal genetic disorders of the phagocytic NADPH oxidase system involved in host defence against various microorganisms. It is manifested by a common phenotype consisting of recurrent serious, life-threatening infection and granuloma formation. Following the finding that interferon gamma-1b (IFNγ-1b) can potentiate phagocyte activity in some other disease states as well as restoring defective phagocyte NADPH oxidase… 

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Partial Correction of the Phagocyte Defect in Patients with X-Linked Chronic Granulomatous Disease by Subcutaneous Interferon Gamma

The efficacy of interferon gamma, a physiologic activator of phagocytic-cell function, in the treatment of chronic granulomatous disease was examined, resulting in 5- to 10-fold increases in superoxide production by granulocytes and monocytes.

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For patients with chronic granulomatous disease, interferon gamma therapy is an effective and well-tolerated treatment that reduces the frequency of serious infections.

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This patient's treatment illustrates the usefulness of the single-photon emission computed tomography (SPECT) gallium scan for following pulmonary inflammatory lesions in the presence of fibrosis and indicates that rHuIFN-gamma may be of benefit to CGD patients with serious infections unresponsive to conventional therapy.

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Although phagocytes from patients with chronic granulomatous disease ingest microorganisms normally, killing is deficient because of the failure of a membrane-associated NADPH oxidase to produce superoxide and related toxic oxygen metabolites, which account for the morbidity and mortality associated with this disease.

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A partial correction in vivo of CGD patients' phagocyte defect with recombinant human interferon-gamma is demonstrated, suggesting that a significant proportion of patients with CGD will respond to rHuIFN-Gamma with augmentation of phagocytes microbicidal function.

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A 19-year-old black man presented with an autosomal recessive form of chronic granulomatous disease (CGD) of childhood (47-kd cytosol protein deficiency) as indicated by a failure of his stimulated neutrophils to consume oxygen or produce hydrogen peroxide and by defective in vitro killing of superoxide.

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The recent genetic and biochemical findings provide an explanation for the consistent absence of the b-cytochrome spectrum in X-CGD, and establish this cytochrome as an essential component of the phagocyte oxidase.

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Restoration of phagocyte function by interferon-gamma in X-linked chronic granulomatous disease occurs at the level of a progenitor cell.

Results indicate that INF-gamma can reprogram the myeloid progenitor cells to express a partially corrected phenotype, and this corrected phenotype is later expressed in daughter cells.

Recombinant interferon gamma augments phagocyte superoxide production and X-chronic granulomatous disease gene expression in X-linked variant chronic granulomatous disease.

Treatment of cultured monocytes from an IFN-gamma-responsive CGD patient increased the steady state level of RNA transcripts from the X-CGD gene from barely detectable up to approximately 5% of normal, and the cytochrome b spectrum remained undetectable.