Allergen‐directed expression of Fc receptors for IgE (CD23) on human T lymphocytes is modulated by interleukin 4 and interferon‐γ

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Abstract
T lymphocytes bearing Fc receptors (FcR) for immunoglobulins are known to have immunoglobulin class-specific regulatory functions. Here we report that expression on T cells of the low-affinity FcR for IgE (FcϵRII/CD23) is preferentially induced by stimulation with antigens that cause an IgE response. T cells from eight patientsallergic to the hemoglobin of Chironomus thummi thummi mosquito larvae (CHIT I) were analyzed for reactivity with the anti-FcERII/CD23 monoclonal antibody (mAb)M-L25 under various conditions. No FcϵRII/CD23+ T cells were observed among freshly isolated, resting peripheral blood mononuclear cells (PBMC). Stimulation of PBMC with CHIT I, however, induced a marked although transient FcϵRII/CD23 expression on a large portion of the allergen-activated T lymphocytes. It reached a maximum of 37.2 ± 4.6% FcϵRII/CD23+ T cell blasts on day 5 of culture. The selectivity of this expression became evident when compared to non-allergenic control antigens: after stimulation of PBMC with tetanus toxoid or purified protein derivative from tuberculin a maximum of 4.6% ± 1.4% and 4.2% ± 1.1% T cell blasts was found to express FcϵRII/CD23, respectively. Activation by an anti-CD3 mAb was insufficient to induce FcϵRII/CD23 on T cells. The allergen-stimulated FcϵRII/CD23+ T cells exclusively belonged to the CD4+CD29+ helper inducer T cell subset. Using a cDNA probe coding for the B cell FcϵRII/CD23, Northern blot analysis revealed a 1.7-kb FcϵRII/CD23 mRNA in extracts of highly purified allergen-stimulated T cells. It was of the same size as FcϵRII/CD23 mRNA of the lymphoblastoid B cell line WI-L2. Of several cytokines tested [interleukin (IL) 1 to IL 6, interferon-γ (IFN-γ), tumor necrosis factor-α] only IL 4 and IFN-γ significantly modified allergen-induced FcϵRII/CD23 expression onT cells. The latter was enhanced nearly twofold in the presence of IL 4, and was almost completely abrogated by IFN-γ. IL 4, however, could not increase the number of FcϵRII/CD23+ T lymphocytes either alone or in combination with an anti-CD3 mAb. Taken together, the selective induction of FcϵRII/CD23 onT cells by allergen and its inclusion in the regulatory network of cytokines point to an important role of FcϵRII/CD23+ T lymphocytes in the human IgE response.