In this study, we describe the interaction between cytokine and cytokine receptor (R) for the activation and proliferation of gamma delta T-cell receptor-positive T cells (gamma delta T cells), gamma delta T cells isolated from murine intestinal intraepithelial lymphocytes (IELs) were separated into gamma delta(Dim) and gamma delta(Bright) fractions according to the intensity of gamma delta T-cell receptor expression, The gamma delta(Dim) T cells express low levels of IL-2R and IL-7R as shown by flow cytometry and reverse transcriptase-PCR analysis, whereas gamma delta(Bright) T cells did not express either receptor, Our study also revealed that recombinant murine (rm)IL-2 and rmIL-7 reciprocally induced high expressions of IL-7R and IL-2R, respectively, on gamma delta(Dim) T cells but not on gamma delta(Bright) IELs. Thus, treatment of gamma delta(Dim) T cells with rmIL-2 and rmIL-7 resulted in high proliferative responses, whereas gamma delta(Bright) T cells did not respond to these two cytokines, The sources of these two cytokines for gamma delta(Dim) T cells were neighboring epithelial cells (IL-7) and alpha beta IELs (IL-2 and IL-7), Cytokine signaling by IL-2 and IL-7 from alpha beta T cells and epithelial cells was necessary for the expression of IL-7R and IL-2R, respectively, on a subset of gamma delta T cells (e.g., gamma delta(Dim) T cells) in mucosa-associated tissue for subsequent activation and cell division.