Absence of the IL-7 receptor component CDw127 indicates that gamma(c) expression alone is insufficient for IL-7 to modulate human neutrophil responses.

It has been proposed that neutrophils are targets for interleukin-7 (IL-7) because this cytokine was found to increase the number of murine immature neutrophils in vivo. In addition, some nonhuman myeloid cell lines were shown to express the IL-7 receptor (IL-7R). Moreover, it was recently discovered that human neutrophils constitutively express the common gamma chain (gamma(c)), known to be a component of not only IL-7R, but also IL-2R, IL-4R, IL-9R, and IL-15R. Among these, we have recently observed that IL-4 and IL-15 are neutrophil agonists. All of the above observations prompted us to study IL-7-human neutrophil interactions. In this study, we investigated potential effects of IL-7 on a range of neutrophil responses. Although we were able to confirm the presence of the gamma(c) component on human neutrophils, we report, for the first time, that these cells lack the CDw127 component of IL-7R. When studying potential modulatory effects of IL-7 on human neutrophils, we found that IL-7 does not induce respiratory burst, phagocytosis, or cytoskeletal functions and does not alter gene expression. Positive controls were included in each assay and the expected results were obtained. In addition, in contrast to IL-4 and IL-15, we found that neutrophil apoptosis is not modulated by IL-7, while granulocyte-macrophage colony-stimulating factor, used here as control, strongly delayed this process as expected. We conclude that the sole expression of gamma(c) on human neutrophils is insufficient to modulate neutrophil responses with respect to the studied functions. Therefore, it cannot be proposed, based on studies performed with nonhuman cells or cell lines, that human neutrophils are targets for IL-7.