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Plaque-forming cell capability in the senescent.

P Tauris, P Andersen, S E Christiansen

    Immunology Letters
    |January 1, 1985
    PubMed
    Summary
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    Aging reduces peripheral blood lymphocytes (PBL) and impairs B cell function. However, aged T cells, when irradiated, enhance plaque-forming cell (PFC) responses in B cells, indicating preserved T helper function.

    Area of Science:

    • Immunology
    • Gerontology
    • Cell Biology

    Background:

    • Aging is associated with a decline in immune function, including reduced lymphocyte counts and altered B cell activity.
    • Understanding age-related changes in immune cell subpopulations is crucial for addressing immune senescence and developing interventions.

    Purpose of the Study:

    • To compare the plaque-forming cell (PFC) response in cultures of peripheral blood lymphocytes (PBL) from healthy aged and young individuals.
    • To investigate the function of T and B cell subpopulations in aged versus young subjects, particularly concerning immunoglobulin secretion.

    Main Methods:

    • Peripheral blood lymphocytes (PBL) from aged and young donors were activated with pokeweed mitogen (PWM).
    • T and B cell subpopulations were separated, reconstituted, and co-cultured.

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  • Protein A PFC assay was used to quantify IgM, IgG, and IgA secretion.

    • Main Results:

    • Aged individuals showed a 36% reduction in PBL and a 27% decrease in sheep erythrocyte-rosette-forming cells (E-RFC).
    • Total PFC numbers were 58% lower in aged PBL cultures compared to young controls.
    • Irradiated aged T cells significantly enhanced PFC responses in co-cultures with B cells (104% increase), while untreated aged T cells showed normal T helper function.

    Conclusions:

    • Aging is characterized by reduced PBL numbers, impaired B cell function, and a distinct enhancement of PFC response when aged T cells are irradiated.
    • The T helper function of untreated aged T cells appears normal, suggesting specific regulatory mechanisms are affected by irradiation in aged T cells.