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      Testing the anti-osteoclastic function of biologic DMARDs

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      Nature Reviews Rheumatology
      Springer Nature

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          CTLA-4 directly inhibits osteoclast formation.

          CTLA-4 is a regulator of co-stimulation and inhibits the activation of T cells through interfering with the interaction of CD80/86 on antigen-presenting cells with CD28 on T cells. CTLA-4 binds to the surface of antigen-presenting cells, such as dendritic cells and monocytes through CD80/86. Monocytes can differentiate in osteoclasts, the primary bone resorbing cells. Herein, we investigated whether the binding of CTLA-4 affects the differentiation of monocytes into osteoclasts in vitro and vivo. We show that CTLA-4 dose-dependently inhibits RANKL- as well as tumour necrosis factor (TNF)-mediated osteoclastogenesis in vitro without the presence of T cells. Furthermore, CTLA-4 was effective in inhibiting TNF-induced osteoclast formation in a non-T cell dependent TNF-induced model of arthritis as well as the formation of inflammatory bone erosion in vivo. These data suggest that CTLA-4 is an anti-osteoclastogenic molecule that directly binds osteoclast precursor cells and inhibits their differentiation. These findings are an attractive explanation for the anti-erosive effect of abatacept, a CTLA-4 immunoglobulin fusion protein used for the treatment of rheumatoid arthritis.
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            Managing rheumatic and musculoskeletal diseases — past, present and future

            The field of rheumatology has seen remarkable progress in the past 70 years. This Perspectives article provides a concise overview of developments in the diagnosis and management of musculoskeletal rheumatic diseases, and what the future of rheumatology might hold.
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              Bone Loss in Rheumatoid Arthritis: Basic Mechanisms and Clinical Implications

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                Author and article information

                Journal
                Nature Reviews Rheumatology
                Nat Rev Rheumatol
                Springer Nature
                1759-4790
                1759-4804
                August 2018
                July 11 2018
                August 2018
                : 14
                : 8
                : 446-448
                Article
                10.1038/s41584-018-0046-0
                4ab24405-627b-4661-b3d4-4eb7c9cd9083
                © 2018

                http://www.springer.com/tdm

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