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Original Article

The Expression of IgE Fc Receptors on Lymphocytes of Allergic Patients

Pages 63-74 | Published online: 10 Jul 2009
 

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.

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