Under both physiological and pathological conditions, bone volume is determined by the rate of bone formation by osteoblasts and bone resorption by osteoclasts. Excessive bone loss is a common complication of human IBD whose mechanisms are not yet completely understood. Despite the role of activated CD4(+) T cells in inflammatory bone loss, the nature of the T cell subsets involved in this process in vivo remains unknown. The aim of the present study was to identify the CD4(+) T cell subsets involved in the process of osteoclastogenesis in vivo, as well as their mechanism of action. CD4(+) T cells were studied in IL10-/- mice and Rag1-/- mice adoptively transferred with naive CD4(+)CD45RB(high) T cells, representing two well-characterised animal models of IBD and in patients with Crohn’s disease. They were phenotypically and functionally characterised by flow cytometric and gene expression analysis, as well as in in vitro cocultures with osteoclast precursors.
The authors, (Thomas Ciucci, Lidia Ibáñez, Agathe Boucoiran, Eléonore Birgy-Barelli, Jérôme Pène, Grazia Abou-Ezzi, Nadia Arab, Matthieu Rouleau, Xavier Hébuterne, Hans Yssel, Claudine Blin-Wakkach, Abdelilah Wakkach) as published in, Gut 2014 October 8, showed that bone marrow Th17 TNFα cells induce osteoclast differentiation, thereby linking bone destruction to IBD and Crohn’s disease.