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Related Experiment Videos

Suppressor monocytes in human disease: a review.

G P Schechter, L M Wahl, J J Oppenheim

    Advances in Experimental Medicine and Biology
    |January 1, 1979
    PubMed
    Summary

    Suppressor monocytes, implicated in diseases like Hodgkin's disease, show impaired function and reduced lymphocyte activating factor (LAF) production. Prostaglandin overproduction may contribute but isn't the sole cause of immune suppression.

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    Area of Science:

    • Immunology
    • Cell Biology
    • Pathology

    Background:

    • Suppressor monocytes are linked to human diseases characterized by lymphopenia and impaired cell-mediated immunity.
    • Quantitative and qualitative monocyte abnormalities are observed in advanced Hodgkin's disease and tuberculosis.

    Purpose of the Study:

    • To investigate the role and mechanisms of suppressor monocytes in specific human diseases.
    • To explore the relationship between monocyte function, lymphocyte activating factor (LAF) production, and prostaglandin secretion.

    Main Methods:

    • Analysis of monocyte function in patients with advanced Hodgkin's disease and tuberculosis.
    • Assessment of lymphocyte activating factor (LAF) production by monocytes.
    • Measurement of prostaglandin secretion from mononuclear cell cultures.
    • Evaluation of indomethacin's effect on monocyte suppression.

    Main Results:

    • Patients exhibited depressed monocyte lymphocyte activating factor (LAF) production, partly due to suppressed T cells.
    • Excessive prostaglandin secretion was noted in some Hodgkin's disease patients, but its association with monocyte suppression was inconsistent.
    • Inhibition of prostaglandin synthetase with indomethacin did not consistently reverse monocyte suppression.

    Conclusions:

    • Suppressor monocyte dysfunction, including impaired LAF production, is evident in certain diseases.
    • Excessive prostaglandin production is unlikely the sole mechanism driving monocyte-induced lymphoproliferation inhibition.
    • Further research is needed to clarify the in vivo relevance of observed in vitro mechanisms, such as effects on delayed hypersensitivity, tumor cytostasis, and cytolysis.

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