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. 2018 Mar 7;57(6):1105–1114. doi: 10.1093/rheumatology/kex525

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Published by Oxford University Press on behalf of the British Society for Rheumatology 2018. This work is written by US Government employees and is in the public domain in the US.

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Fig. 5 — Model of MR1-induced bone anabolism

(A) Immune responses initiated by engagement of APC expressing antigen as part of MHCI (CD8⁺ T cells) or MHCII (CD4⁺ T cells). (B) A costimulatory signal is necessary for T cell activation and provided by T cell CD28 binding to APC CD80/86. (C) CD40L on activated T cells associates with APC CD40. (D) MR1 blocks CD40/CD40L costimulation causing differentiation of FoxP3⁺ Tregs and cytotoxic T lymphocyte antigen 4 (CTLA-4) secretion disrupting CD28 costimulation causing T cell anergy. (E) Anergic CD8⁺ T cells produce Wnt-10b, a bone anabolic factor. (F) Wnt-10b binds to receptors (LRP5/6) on osteoblast lineage cells, promoting bone formation. APC: antigen presenting cell; MHC: major histocompatibility complex.