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Abstract
Bone and immune system are functionally interconnected. Immune and bone cells derive from same progenitors in the bone marrow, they share a common microenvironment and are being influenced by similar mediators. The evidence on increased bone resorption associated with inappropriate activation of T cells such as during inflammation, is well established. However, the molecular mechanisms beyond this clinical observation have begun to be intensively studied with the advancement of osteoimmunology. Now days, we have firm evidence on the influence of numerous proinflammatory cytokines on bone cells, with the majority of data focused on osteoclasts, the bone resorbing cells. It has been shown that some proinflammatory cytokines could possess osteoclastogenic and/or anti-osteoclastogenic properties and can target osteoclasts directly or via receptor activator of nuclear factor κB (RANK)/RANK ligand(RANKL)/osteoprotegerin (OPG) system. Several studies have reported opposing data regarding (anti)osteoclastogenic properties of these cytokines.Therefore, the first part of this review is summarizing current evidence on the influence of pro-inflammatory cytokines on osteoclasts and thus on bone resorption. In the second part, the evidence on the role of pro-inflammatory cytokines in osteoporosis and osteoarthritis is reviewed to show that unravelling the mechanisms beyond such complex bone diseases, is almost impossible without considering skeletal and immune systems as an indivisible integrated system.
Highlights
It is well established that bone and immune cells are functionally connected
IL-8 belongs to a group of chemokines and is, unlike other osteoclastogenic cytokines that we have described up to this point, produced by T cells and macrophages and by osteoclasts themselves
In this study we found higher expression of genes encoding for IL-1α, IL-6, RANKL and RANK in osteoporotic bone tissue
Summary
It is well established that bone and immune cells are functionally connected. Diverse interactions between bone and immune cells occur within the bone microenvironment. We have to take in account that pro-inflammatory cytokines such as TNF-α and IL-17, released from activated T cells, can target osteoblasts as well The result of such influence is the increased production of pro-inflammatory cytokines and RANKL in osteoblasts and the contribution of these cells to bone resorption [4]. IFN-γ binds to its receptor on osteoclasts, degrades RANKL signaling and inhibits the activation of osteoclasts and protects our bones from being resorbed This cytokine is produced predominantly by NK and natural killer T (NKT) cells involved in the innate immune response, and by CD4+ Th1 and CD8+ cytotoxic T lymphocyte (CTL) effector T cells, once antigen-specific immunity develops [12]. Up to date evidence on the role of pro-inflammatory cytokines in OP and OA will be summarized, with the aim to show that researching such complex bone disorders is almost impossible without considering skeletal and immune system in an integrated way
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