T-Cell Mediated Inflammation in Postmenopausal Osteoporosis

Wu, Di; Cline-Smith, Anna; Shashkova, Elena V.; Perla, Ajit; Katyal, Aditya; Aurora, Rajeev

doi:10.3389/fimmu.2021.687551

Cited by 79 publications

(75 citation statements)

References 130 publications

(130 reference statements)

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“…Bone remodelling starts with the destruction of old bone by osteoclasts followed by the deposition of osteoids by osteoblasts within basic multicellular units (BMUs), which are composed of osteoclasts, osteoblasts and the capillary blood supply. Subsequently, the organic extracellular matrix is mineralized [ 16 , 18 ]. This process, which occurs throughout life, may replace microdamage and ensure structural integrity.…”

Section: Pathological Mechanism Of Osteoporosismentioning

confidence: 99%

STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis

Hou

Tian

2022

Cell Commun Signal

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Osteoporosis is a common skeletal disease with marked bone loss, deterioration of the bone microstructure and bone fragility. An abnormal bone remodelling cycle with relatively increased bone resorption is the crucial pathophysiological mechanism. Bone remodelling is predominantly controlled by osteoblasts and osteoclasts, which are specialized cell types that are regulated by a variety of osteogenic and osteoclastic factors, including cytokines expressed within the bone microenvironment under local or systemic inflammatory conditions. Signal transducer and activator of transcription 3 (STAT3) plays a prominent role in the communication between cytokines and kinases by binding downstream gene promotors and is involved in a wide range of biological or pathological processes. Emerging evidence suggests that STAT3 and its network participate in bone remodelling and the development of osteoporosis, and this factor may be a potent target for osteoporosis treatment. This review focuses on the role and molecular mechanism of the STAT3 signalling pathway in osteogenesis, osteoclastogenesis and osteoporosis, particularly the bone-related cytokines that regulate the osteoblastic differentiation of bone marrow stromal cells and the osteoclastic differentiation of bone marrow macrophages by initiating STAT3 signalling. This review also examines the cellular interactions among immune cells, haematopoietic cells and osteoblastic/osteoclastic cells.

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Section: Pathological Mechanism Of Osteoporosismentioning

confidence: 99%

STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis

Hou

Tian

2022

Cell Commun Signal

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“…Recently, a new pathway has been described, indicating that E2 loss results in chronic production of TNF-α and IL-17 by converting T M into T E . IL-7 and IL-15 are involved in the process; both are mainly secreted by bone marrow dendritic cells (BMDCs), which are important APCs in the bone marrow (BM) ( 15 ). Animal experiments have shown the absence of bone loss in specially treated mice, in which T M cannot convert into T E ( 16 ).…”

Section: E2 Deficiency Leads To Conversion Of T Cells Into T ...mentioning

confidence: 99%

Role of the major histocompatibility complex class II protein presentation pathway in bone immunity imbalance in postmenopausal osteoporosis

et al. 2022

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Bone immunity regulates osteoclast differentiation and bone resorption and is a potential target for the treatment of postmenopausal osteoporosis (PMOP). The molecular network between bone metabolism and the immune system is complex. However, the molecular mechanism underlying the involvement of the major histocompatibility complex class II (MHC-II) molecule protein presentation pathway in PMOP remains to be elucidated. The MHC-II molecule is a core molecule of the protein presentation pathway. It is combined with the processed short peptide and presented to T lymphocytes, thereby activating them to become effector T cells. T-cell-derived inflammatory factors promote bone remodeling in PMOP. Moreover, the MHC-II molecule is highly expressed in osteoclast precursors. MHC-II transactivator (CIITA) is the main regulator of MHC-II gene expression and the switch for protein presentation. CIITA is also a major regulator of osteoclast differentiation and bone homeostasis. Therefore, we hypothesized that the MHC-II promotes osteoclast differentiation, providing a novel pathogenic mechanism and a potential target for the treatment of PMOP.

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“…On the other hand, during osteoporosis, inflammatory mediators such as pro-inflammatory cytokines act on the skeletal cells directly or indirectly to promote the development of osteoporosis ( McLean, 2009 ). Besides, recent evidence suggests both innate and adaptive immunocytes contribute to osteoporosis ( Saxena et al, 2021 ; Wu et al, 2021 ).…”

Section: Pathogenesis and Molecular Mechanisms Of Osteoporosismentioning

confidence: 99%

HO-1 in Bone Biology: Potential Therapeutic Strategies for Osteoporosis

Zhou

Yuan

Xiong

et al. 2021

Front. Cell Dev. Biol.

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Osteoporosis is a prevalent bone disorder characterized by bone mass reduction and deterioration of bone microarchitecture leading to bone fragility and fracture risk. In recent decades, knowledge regarding the etiological mechanisms emphasizes that inflammation, oxidative stress and senescence of bone cells contribute to the development of osteoporosis. Studies have demonstrated that heme oxygenase 1 (HO-1), an inducible enzyme catalyzing heme degradation, exhibits anti-inflammatory, anti-oxidative stress and anti-apoptosis properties. Emerging evidence has revealed that HO-1 is critical in the maintenance of bone homeostasis, making HO-1 a potential target for osteoporosis treatment. In this Review, we aim to provide an introduction to current knowledge of HO-1 biology and its regulation, focusing specifically on its roles in bone homeostasis and osteoporosis. We also examine the potential of HO-1-based pharmacological therapeutics for osteoporosis and issues faced during clinical translation.

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T-Cell Mediated Inflammation in Postmenopausal Osteoporosis

Cited by 79 publications

References 130 publications

STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis

STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis

Role of the major histocompatibility complex class II protein presentation pathway in bone immunity imbalance in postmenopausal osteoporosis

HO-1 in Bone Biology: Potential Therapeutic Strategies for Osteoporosis

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