Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies

Abstract

Article:El-Zayadi, AA, Jones, EA orcid.org/0000-0001-9365-2283, Churchman, SM orcid.org/0000-0003-0172-3975 et al. (7 more authors) (2017) Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies. Rheumatology, 56 (3 ReuseUnless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request. This is a Conclusion. This work shows that IL-22 is involved in human MSC proliferation/migration in inflammatory environments with MSC osteogenesis occurring only in IFN-/TNF absence. These effects of IL-22 on MSC function is a novel pathway for exploring pathological, post-inflammation osteogenesis in human SpA.

Optimising proliferation and migration of mesenchymal stem cells using platelet products: A rational approach to bone regeneration

“…26 TNF-a and IL-1b are known to induce inflammation causing a biphasic physiological response; whilst inflammation is necessary for healing, 43 in excess it is thought to activate the NFkB pathway 26 inhibiting osteogenesis and pro-moting osteoclastogenesis. 44 However, more recently, these proinflammatory cytokines have been linked to increased osteogenesis, 45 BM-MSC migration, 46 and proliferation 47 indicative of the lack of consensus in the field.…”

The role of IL‐23 receptor signaling in inflammation‐mediated erosive autoimmune arthritis and bone remodeling

“…Similar to IL-23, overexpression of IL-22 leads to new periosteal bone formation through STAT3 activation and increased expression of genes that regulate bone formation, including the Wnt family members [42]. These findings are further supported by a recent study demonstrating that IL-22 stimulates human mesenchymal stem cell proliferation and migration and increases osteogenic genes such as ALPL and Runx2 [83]. Interestingly, IL-23 has also been reported to directly regulate osteoblast formation as its binding to the IL-23R on human mesenchymal stem cells leads to increased expression of osteoblast-related genes and formation of osteoblasts in vitro (Fig.…”

The roles of immune cells in bone healing; what we know, do not know and future perspectives

“…Furthermore, innate lymphocytes cells (ILCs) that produce tissue reparative cytokines such as interleukin-22 (IL-22) [53][54][55] also seem to induce the osteogenic activity of MSCs. Recently, an in vitro study has shown that IL-22 can induce the osteogenic capacity of licensed BM MSCs [56]. Likewise, once MSCs are licensed, IL-17 induces osteogenesis by increase the expression of osteogenic proteins in MSCs, Cbfa1/Runx2 and collagen [14].I n conclusion, the inflammatory microenvironment delivers important signals that help the preparation of MSCs, proliferation and immunomodulation and then the osteogenesis.…”