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  • Title: In vitro production of IgE by human peripheral blood mononuclear cells. II. Cells involved in the spontaneous IgE production in atopic patients.
    Author: Romagnani S, Del Prete GF, Maggi E, Troncone R, Giudizi GM, Almerigogna F, Ricci M.
    Journal: Clin Exp Immunol; 1980 Dec; 42(3):579-88. PubMed ID: 6971197.
    Abstract:
    Spontaneous IgE production in vitro was investigated in 7-day cultures of unfractionated mononuclear cells (MNC) and MNC subpopulations from atopic patients. Depletion of either phagocytic or adherent cells decreased the amount of IgE detectable in 7-day culture supernatants, but this decrease was due, at least in part, to a loss of cytophilic IgE. Depletion of immunoglobulin-bearing cells (SIg+) reduced significantly but did not abolish the spontaneous IgE production in vitro. On the other hand, depletion of IgM-bearing lymphocytes (SIgM+), which virtually abolished the production of immunoglobulins of the IgM class, did not change significantly the spontaneous production of IgE. Similarly, no change in the spontaneous production of IgE was found when lymphocyte suspensions were depleted of complement receptor-bearing cells (CR+). In contrast, spontaneous IgE production was significantly increased by depletion of T lymphocytes and this increase did not simply reflect the enrichment for IgE-producing cells caused by the fractionation procedure. No significant change in the spontaneous IgE production was found when small numbers of autologous T lymphocytes were added to B cell fractions, whereas the addition of higher concentrations of autologous T cells induced a marked inhibition of the spontaneous IgE production. On the other hand, the addition in culture of pokeweed mitogen (PWM) resulted in a marked reduction of the spontaneous IgE production by B cells, also in the presence of small concentrations of autologous T lymphocytes. Normal T cells were consistently effective in inducing a partial inhibition of the spontaneous IgE production by B cells from atopic patients, whereas T cells from a noticeable proportion of atopic patients were not. These data suggest that MNC responsible for the spontaneous IgE production in atopic subjects are SIgM- and CR-deficient well-differentiated lymphocytes which probably represent the result of an activation which has occurred in vivo. However, this spontaneous IgE production can still be influenced by in vitro manipulation, such as variations in T–B cell ratios or addition of PWM. The results here reported also indicate that normal T cells are generally more effective than T cells from atopic patients in regulating the activity of spontaneous IgE-producing cells present in the blood of atopic subjects.
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