Role of γ/δT cells in a patient with CD4+CD3- lymphocytosis, hypereosinophilia, and high levels of IgE

Ilan Bank*, Avner Reshef, Miriam Beniaminov, Ester Rosenthal, Gideon Rechavi, Yehudit Monselise

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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 lU/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-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. Conclusions: 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.

Original languageEnglish
Pages (from-to)621-630
Number of pages10
JournalJournal of Allergy and Clinical Immunology
Issue number4 II
StatePublished - 1998


  • CD4 T cells
  • Hypereosinophilic syndrome
  • IFN-γ
  • IL-4
  • γδ T cells


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