ROLE OF GAMMA DELTA T-CELLS IN A PATIENT WITH CD4(+)CD3(-) LYMPHOCYTOSIS, HYPEREOSINOPHILIA, AND HIGH-LEVELS OF IGE/

Background: CD4(+)CD3(-) T cells have previously been shown to play a pathogenic role in the hypereosinophilic syndrome by secreting IL-5 an d IL-4. Objectives: The goal of this study was to study the role of CD 4+CD3- and other T-cell subsets in a patient with eosinophilia, dermat itis, and a high level of IgE (100,000 IU/mL) in the serum. Methods: W e isolated PBMCs and performed flow cytometry, cell cultures, and in v itro assays of Ig, Lymphokine production, and cell-mediated cytotoxici ty, Results: Flow cytometric and immunohistochemical analysis of the P BMCs revealed a major population (consisting of approximately 85% of t he CD4(+) T cells) that lacked expression of CD3 and T-cell receptors on the cell surface (CD4(+)CD3(-)T cells), but did express CD3 peptide s in the cytoplasm. Activation of the PBMCs in vitro resulted in a 100 -fold greater than normal release of IL-4, whereas IFN-gamma productio n was less than normal, suggesting a predominantly type 2 helper funct ional phenotype of the CD4+CD3- T cells. Importantly, both CD4(-)CD8(l ow) V delta 1(+) T-cell receptor gamma delta(+) and CD4(+)CD3(-) T cel ls were cultured from the PBMCs, The former secreted IFN-gamma exclusi vely, whereas the latter secreted both IL-4 and IFN-gamma. Furthermore , only the T-cell receptor gamma delta(+) lymphocytes were cytotoxic t o autologous B-lymphoblastoid cells and specifically inhibited IgE pro duction in cultures of autologous polyclonally stimulated PBMCs, Concl usions: The results suggest that CDloq V delta 1(+) T cell receptor ga mma delta(+) clones functionally counteract IgE-inducing effects of ty pe 2 CD4+CD3- helper cells in this patient with hypereosinophilic synd rome.