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Osteoimmunology in Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Lia Ginaldi, Daniela Di Silvestre, Maria Maddalena Sirufo, Massimo De Martinis
An unexpected relationship between bone and immune cells has recently emerged, resulting in the establishment of osteoimmunology, an innovative discipline that investigates interactions between the skeleton and immune system, the so-called immunoskeletal interface. Recent discoveries in this research field highlighted a new landscape of osteoporosis, and enabled the development of innovative therapies for its treatment. From this perspective, osteoporosis could be regarded as an age-related chronic immune-mediated disease, sharing with other age-related disorders a common inflammatory background [1].
Osteocalcin and regulatory cytokine imbalance in children with congenital cleft lip and palate
Published in Immunological Medicine, 2020
Irina Nesterova, Marina Mitropanova, Galina Chudilova, Lyudmila Lomtatidze
Over the past decade, a new scientific direction, osteoimmunology, has been actively developed [11]. Osteoimmunology is an interdiscipline that focuses on the relationship between the skeletal and immune systems. In 2000, Arron J. and Choi Y. first proposed the term ‘osteoimmunology’ [12]. Over the past 20 years, evidence has accumulated demonstrating that the skeletal system is involved in the processes of hematopoiesis and affects the state of the immune system. At the same time, numerous cells of the immune system and the cytokines produced by them are involved in bone homeostasis. Complex interactions between the bone and immune systems occur in various diseases, such as osteoporosis, rheumatoid arthritis, ankylosing spondylitis, HIV infection, Crohn’s disease, systemic lupus erythematosus [13–16]. Cells of the immune system regulate bone cells using various cytokines and molecules. It is known that IL1β, IL6, IL17, TNFα, TNFβ, RANKL and M-CSF promote osteoclastogenesis. Molecules IL23, IL6, IL12, IL18, IL4, IFNγ and TGFβ inhibit osteoclastogenesis, IL17A and BMP-2 stimulate the formation of osteoblasts [11].
The role of imaging in early diagnosis and prevention of joint damage in inflammatory arthritis
Published in Expert Review of Clinical Immunology, 2018
Jiang Yue, Dongze Wu, Lai-Shan Tam
Bone homeostasis, which involves osteoblast and osteoclast, is an important process for maintaining adequate bone mass in humans. Inflammatory burden and autoantibody positivity have both been identified as important initiators of skeletal damage in arthritis. Osteoimmunology is important in helping us understand the interaction between the skeletal and the immune systems. Unraveling the cellular and molecular mechanisms elicited by synovial cytokine networks that dictate recruitment, differentiation, and activation of osteoclast precursors and osteoclasts, respectively, is central to shaping novel therapeutic options for inflammatory arthritis patients. With the availability of various imaging modalities including US, MRI, and HR-pQCT, these powerful tools are becoming more important to assist clinicians in early detection of inflammation and joint destruction. Nonetheless, the clinical utility of these imaging tools to improve diagnostic accuracy and guiding therapeutic decision-making is still unclear.
The role of macrophages and osteoclasts in the progression of leukemia
Published in Hematology, 2021
Kun Li, Runming Jin, Xiaoyan Wu
Over the years, leukemia is considered to be a series of genetic attacks on hematopoietic stem/progenitor cells (HSPCs), which convert them into preleukemic and eventually into leukemic cells. Recent findings suggest that genetic changes in niche cells, particularly in osteogenic cells, may also result in leukemia in a mouse model[17,48]. The osteogenic niche is mainly composed of OBs, osteocytes and OCs, and plays a key role in the maintenance and expansion of HSPCs as well as in their transformation into leukemia cells. Bone is one of most common sites for metastasis, often leading to mortality. Matrix metalloproteinases (MMPs) expressed at the interface between tumor and stromal cells play an important role in osteolysis and dissemination into bone tissue. MMP-7 expressed by osteoclasts at the tumor-bone interface triggers osteolysis and subsequent bone metastasis in a rodent model of prostate cancer[49]. An increasing number of studies have proven that bone is also an immune organ with important immune regulation functions. Bone not only provides the structural framework of the body but also acts as a reservoir for hematopoietic cells and immune cells[31,48]. Hematopoietic cells, immune cells, osteoblasts, osteoclasts and other cells share the BMME. In recent years, a better understanding has been reached on the interaction mechanism between bone and the immune system, and a new cross-disciplinary osteoimmunology has been developed. Bone immunological studies have shown that T cells play an important role in the mediation of osteoclasts. On the one hand, activated T lymphocytes are an important source of RANKL and IL-1β, which are important activating factors for osteoclasts, thereby activating osteoclasts, which has also been observed in rheumatoid arthritis; on the other hand, activated T lymphocytes can also secrete IFN-γ, IL-4, IL-10 and other cytokines to inhibit osteoclasts[31]. Therefore, normally functioning T cells play an important role in regulating the balance of bone metabolism.