Abstract:
:Bone destruction relies on interactions between bone and immune cells. Bone-resorbing osteoclasts (OCLs) were recently identified as innate immune cells activating T cells toward tolerance or inflammation. Thus, pathological bone destruction not only relies on increased osteoclast differentiation, but also on the presence of inflammatory OCLs (i-OCLs), part of which express Cx3cr1. Here, we investigated the contribution of mouse Cx3cr1+ and Cx3cr1neg i-OCLs to bone loss. We showed that Cx3cr1+ and Cx3cr1neg i-OCLs differ considerably in transcriptional and functional aspects. Cx3cr1neg i-OCLs have a high ability to resorb bone and activate inflammatory CD4+ T cells. Although Cx3cr1+ i-OCLs are associated with inflammation, they resorb less and have in vitro an immune-suppressive effect on Cx3cr1neg i-OCLs, mediated by PD-L1. Our results provide new insights into i-OCL heterogeneity. They also reveal that different i-OCL subsets may interact to regulate inflammation. This contributes to a better understanding and prevention of inflammatory bone destruction.
journal_name
Elifejournal_title
eLifeauthors
Madel MB,Ibáñez L,Ciucci T,Halper J,Rouleau M,Boutin A,Hue C,Duroux-Richard I,Apparailly F,Garchon HJ,Wakkach A,Blin-Wakkach Cdoi
10.7554/eLife.54493subject
Has Abstractpub_date
2020-05-13 00:00:00issn
2050-084Xpii
54493journal_volume
9pub_type
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