Role of γ/δ T cells in a patient with CD4+CD3− lymphocytosis, hypereosinophilia, and high levels of IgE

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CD4+CD3− T cells have previously been shown to play a pathogenic role in the hypereosinophilic syndrome by secreting IL-5 and IL-4.


The goal of this study was to study the role of CD4+CD3− and other T-cell subsets in a patient with eosinophilia, dermatitis, and a high level of IgE (100,000 IU/mL) in the serum.


We isolated PBMCs and performed flow cytometry, cell cultures, and in vitro assays of Ig, lymphokine production, and cell-mediated cytotoxicity.


Flow cytometric and immunohistochemical analysis of the PBMCs revealed a major population (consisting of approximately 85% of the CD4+ T cells) that lacked expression of CD3 and T-cell receptors on the cell surface (CD4+CD3− T cells), but did express CD3 peptides in the cytoplasm. Activation of the PBMCs in vitro resulted in a 100-fold greater than normal release of IL-4, whereas IFN-γ production was less than normal, suggesting a predominantly type 2 helper functional phenotype of the CD4+CD3− T cells. Importantly, both CD4−CD8low Vδ1+ T-cell receptor γδ+ and CD4+CD3− T cells were cultured from the PBMCs. The former secreted IFN-γ exclusively, whereas the latter secreted both IL-4 and IFN-γ. Furthermore, only the T-cell receptor γδ+ lymphocytes were cytotoxic to autologous B-lymphoblastoid cells and specifically inhibited IgE production in cultures of autologous polyclonally stimulated PBMCs.


The results suggest that CD8low Vδ1+ T-cell receptor γδ+ clones functionally counteract IgE-inducing effects of type 2 CD4+CD3− helper cells in this patient with hypereosinophilic syndrome.

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