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Macrophage-lymphocyte interactions mediated by soluble factors.

H B Herscowitz, K J Pennline, R E Conrad

    Annals of the New York Academy of Sciences
    |January 1, 1979
    PubMed
    Summary

    Rabbit alveolar macrophages (AM) suppress antibody-producing cell responses but enhance responses to mitogens. This dual activity is mediated by a soluble factor dependent on RNA synthesis, impacting lymphocyte proliferation.

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    Area of Science:

    • Immunology
    • Cell Biology
    • Macrophage Function

    Background:

    • Splenocytes are crucial for mounting immune responses.
    • Alveolar macrophages (AM) play a role in lung immunity.
    • The immunomodulatory functions of AM require further elucidation.

    Purpose of the Study:

    • To investigate the effect of rabbit alveolar macrophages (AM) on splenocyte immune responses.
    • To characterize the suppressive and enhancing activities of AM.
    • To identify the mechanisms underlying AM-mediated immunomodulation.

    Main Methods:

    • In vitro culture of primed rabbit splenocytes.
    • Addition of alveolar macrophages (AM) to lymphocyte populations.
    • Assessment of plaque-forming cell (PFC) response to SRBC.

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  • Analysis of lymphocyte proliferation in response to mitogens (PHA, Con A).
  • Characterization of suppressive factors (irradiation, heat, chemical treatments).

    • Main Results:

    • Alveolar macrophages (AM) significantly suppressed the PFC response in a dose-dependent manner (1 AM:20 lymphocytes).
    • Suppressive activity was mediated by a soluble factor (>10,000 MW) requiring AM-lymphocyte interaction and RNA synthesis.
    • AM enhanced lymphocyte proliferation to PHA and Con A, also dependent on RNA synthesis.

    Conclusions:

    • Rabbit alveolar macrophages (AM) possess both suppressive and enhancing immunomodulatory functions.
    • Suppression of antibody response and enhancement of mitogen response are linked to RNA synthesis.
    • AM influence antigen-sensitive cell proliferation and early immune events.