BACKGROUND: CD4+CD3- T cells have previously been shown to play a pathogenic role in the hypereosinophilic syndrome by secreting IL-5 and IL-4. OBJECTIVES: 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. METHODS: We isolated PBMCs and performed flow cytometry, cell cultures, and in vitro assays of Ig, lymphokine production, and cell-mediated cytotoxicity. RESULTS: 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-gamma production was less than normal, suggesting a predominantly type 2 helper functional phenotype of the CD4+CD3- T cells. Importantly, both CD4-CD8(low) Vdelta1+ T-cell receptor gammadelta+ and CD4+CD3- T cells were cultured from the PBMCs. The former secreted IFN-gamma exclusively, whereas the latter secreted both IL-4 and IFN-gamma. Furthermore, only the T-cell receptor gammadelta+ lymphocytes were cytotoxic to autologous B-lymphoblastoid cells and specifically inhibited IgE production in cultures of autologous polyclonally stimulated PBMCs. CONCLUSIONS: The results suggest that CD8(low) Vdelta1+ T-cell receptor gammadelta+ clones functionally counteract IgE-inducing effects of type 2 CD4+CD3- helper cells in this patient with hypereosinophilic syndrome.
BACKGROUND:CD4+CD3- T cells have previously been shown to play a pathogenic role in the hypereosinophilic syndrome by secreting IL-5 and IL-4. OBJECTIVES: 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. METHODS: We isolated PBMCs and performed flow cytometry, cell cultures, and in vitro assays of Ig, lymphokine production, and cell-mediated cytotoxicity. RESULTS: 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-gamma production was less than normal, suggesting a predominantly type 2 helper functional phenotype of the CD4+CD3- T cells. Importantly, both CD4-CD8(low) Vdelta1+ T-cell receptor gammadelta+ and CD4+CD3- T cells were cultured from the PBMCs. The former secreted IFN-gamma exclusively, whereas the latter secreted both IL-4 and IFN-gamma. Furthermore, only the T-cell receptor gammadelta+ lymphocytes were cytotoxic to autologous B-lymphoblastoid cells and specifically inhibited IgE production in cultures of autologous polyclonally stimulated PBMCs. CONCLUSIONS: The results suggest that CD8(low) Vdelta1+ T-cell receptor gammadelta+ clones functionally counteract IgE-inducing effects of type 2 CD4+CD3- helper cells in this patient with hypereosinophilic syndrome.