Dysregulated expression of the IL-2 receptor β-chain abrogates development of NK cells and Thy-1+ dendritic epidermal cells in transgenic mice

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Abstract
The IL-2 receptor β-chain (IL-2Rβ), a specificity-determining subunlt In the IL-2R complex with a restricted tissue distribution pattern, Is essential for signal transductlon. Our previous studies demonstrate that the continuous treatment of mice with anti-IL-2Rβ) resulted in the complete disappearance of NK cells and Thy-1+ dendritic epidermal cells (Thy-1+ dEC), suggesting that signals through IL-2Rβ are critically involved in development of these lymphocyte subsets. However, these lymphocyte subsets are reported to be apparently unaffected In the IL-2-deficient mice. To further examine the biological roles of the IL-2Rβ, transgenic mice carrying the IL-2Rβ transgene were generated. In these mice, high levels of the cell surface expression of the IL-2Rβ were observed in essentially all hematopoietic lineage cells, and CD4+ T cells as well as CD8+ T cells showed vigorous cell proliferation upon IL-2 stimulation. Surprisingly, NK cells marked with a high expression of NK1.1 in the spleen and Thy-1+ dEC in the skin were completely absent in transgenic mice. However, the development of other lymphocyte subsets Including conventional αβTCR + cells, γδTCR+ cells and B cells remained apparently intact. From these observations together with previous data on IL-2-deficlent mice, we speculate that factors, other than IL-2 that utilizes the IL-2Rβ as its functional receptor subunlt, may have a vital role in the development of NK cells and Thy-1+ dEC. Implications for possible In vivo functions of over-expressed IL-2Rβ are discussed.

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