Interleukin-7 links T lymphocyte and intestinal epithelial cell homeostasis.
Web of Science
AuthorShalapour, S; Deiser, K; Kühl, AA; Glauben, R; Krug, SM; Fischer, A; Sercan, O; Chappaz, S; Bereswill, S; Heimesaat, MM; ...
Source TitlePLoS One
PublisherPublic Library of Science (PLoS)
University of Melbourne Author/sChappaz, Stephanie
AffiliationMedical Biology (W.E.H.I.)
Document TypeJournal Article
CitationsShalapour, S., Deiser, K., Kühl, A. A., Glauben, R., Krug, S. M., Fischer, A., Sercan, O., Chappaz, S., Bereswill, S., Heimesaat, M. M., Loddenkemper, C., Fromm, M., Finke, D., Hämmerling, G. J., Arnold, B., Siegmund, B. & Schüler, T. (2012). Interleukin-7 links T lymphocyte and intestinal epithelial cell homeostasis.. PLoS One, 7 (2), pp.e31939-. https://doi.org/10.1371/journal.pone.0031939.
Access StatusOpen Access
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3288069
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.
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