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Martin, Christopher E.,Spasova, Darina S.,Frimpong-Boateng, Kwesi,Kim, Hee-Ok,Lee, Minji,Kim, Kwang Soon,Surh, Charles D. Elsevier 2017 Immunity Vol.47 No.1
<P><B>Summary</B></P> <P>Interleukin-7 (IL-7) availability determines the size and proliferative state of the resting T cell pool. However, the mechanisms that regulate steady-state IL-7 amounts are unclear. Using experimental lymphopenic mouse models and IL-7-induced homeostatic proliferation to measure IL-7 availability in vivo, we found that radioresistant cells were the source of IL-7 for both CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T cells. Hematopoietic lineage cells, although irrelevant as a source of IL-7, were primarily responsible for limiting IL-7 availability via their expression of IL-7R. Unexpectedly, innate lymphoid cells were found to have a potent influence on IL-7 amounts in the primary and secondary lymphoid tissues. These results demonstrate that IL-7 homeostasis is achieved through consumption by multiple subsets of innate and adaptive immune cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> IL-7 is produced by radioresistant cells and not by hematopoietic cells </LI> <LI> IL-7R expressed by hematopoietic cells controls IL-7 availability </LI> <LI> ILCs outcompete T cells for IL-7 by resisting IL-7-mediated IL-7R downregulation </LI> <LI> ILCs are more resistant to IL-7-mediated downmodulation of FOXO1 </LI> </UL> </P>
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