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Shabnam Shalapour; Katrin Deiser; Anja A. Kühl; Rainer Glauben; Susanne M. Krug; André Fischer; Özen Sercan; Stephane Chappaz; Stefan Bereswill; Markus M. Heimesaat; et al. (Profiled Author: Peter J. Haemmerling)
PLoS ONE. 2012;7(2).Abstract
Interleukin-7 (IL-7) is a major survival factor for mature T cells. Therefore, the degree of IL-7 availability determines the size of the peripheral T cell pool and regulates T cell homeostasis. Here we provide evidence that IL-7 also regulates the homeostasis of intestinal epithelial cells (IEC), colon function and the composition of the commensal microflora. In the colon of T cell-deficient, lymphopenic mice, IL-7-producing IEC accumulate. IEC hyperplasia can be blocked by IL-7-consuming T cells or the inactivation of the IL-7/IL-7R signaling pathway. However, the blockade of the IL-7/IL-7R signaling pathway renders T cell-deficient mice more sensitive to chemically-induced IEC damage and subsequent colitis. In summary, our data demonstrate that IL-7 promotes IEC hyperplasia under lymphopenic conditions. Under non-lymphopenic conditions, however, T cells consume IL-7 thereby limiting IEC expansion and survival. Hence, the degree of IL-7 availability regulates both, T cell and IEC homeostasis. © 2012 Shalapour et al.
PMID: 22384106 PMCID: PMC3288069
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