The Expression of IgE Fc Receptors on Lymphocytes of Allergic Patients

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Abstract
Peripheral blood lymphocytes from nonatopic subjects and atopic patients were analyzed for cells expressing Fc receptors for IgE (FcϵR). Nonatopic humans and atopic patients in remission had approximately 1 percent of FcϵR+ peripheral blood lymphocytes. Usually >99 percent of these cells were mIgM+/mIgD+ Bcells. However, in approximately 10 percent of nonatopic and atopic subjects a transient increase of FcϵR+ lymphocytes to 3–6 percent was observed in the absence of any disease manifestations and measurable changes in the serum IgE level. At times of increased numbers of peripheral blood FcϵR+ lymphocytes, up to 1 percent FcϵR+ positive cells were detected in isolated T cell preparations. The FcϵR+ T cells reacted with the monoclonal antibody Lyt 3 to the sheep erythrocyte receptor of human T cells but not the anti-T cell antibody OKT3, and fractions also with the monoclonal antibodies OKT8 (cytotoxic and suppressor T cells) and OKM1, which binds to an antigen present on monocytes and a subpopulation of T cells and large granular lymphocytes. No OKT4+ (helper T cells) FcϵR+ cells were detected. The reactivity with monoclonal antibodies to T cell subsets of the FcϵR+ T cells paralleled the reactivity of the IgG Fc receptor positive T cells. In contrast to patients with allergic rhinitis and asthma, patients with severe atopic dermatitis or the Hyper IgE Syndrome always had significantly elevated percentage of FcϵR+ lymphocytes (4–10 percent), which were almost entirely B cells since < 0.1 percent FcϵR+ T cells were delected in these patients. Atopic dermatitis patients receiving systemic corticosteroid treatment had only 0.2 percent FcϵR+ lymphocytes which was significantly less than the 1 percent of the nonatopic control donors. Attempts to define the function of FcϵR on human B and T lymphocytes have been unsuccessful thus far; however, the increase of FcϵR+ cells associated with atopic disease in man and parasitic infections in rats and mice suggest that FcϵR+ lymphocyte may be involved in the IgE isotype regulation.