B cells activated in the presence of Th1 cytokines inhibit osteoclastogenesis

Choi, Youngnim; Kim, Jeong Jae

doi:10.1038/emm.2003.51

Cited by 38 publications

(30 citation statements)

References 23 publications

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“…Even in vitro, osteoclastogenesis did not B occur efficiently in the semisolid culture system (Miyamoto et al, 2000). Furthermore, IFN-γ directed macrophages to differentiate into giant cells rather than osteoclasts in the presence of M-CSF plus RANKL in vitro (Choi and Kim, 2003). Our results indicated that RANKL augments the function of macrophages as antigen presenting cells but not as effector cells.…”

Section: Proinflammatory Cytokines and Inosmentioning

confidence: 64%

Receptor activator of NF-κB ligand enhances the activity of macrophages as antigen presenting cells

Park

Park²,

Shin³

et al. 2005

Exp Mol Med

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Receptor activator of NFκB ligand (RANKL) is known as a key regulator of osteoclastogenesis. However, the fact that fibroblasts and periodontal ligament cells express RANKL in response to bacterial substances, suggests that RANKL may have evolved as a part of the immunity to infection. As RANKL increases the survival and activity of dendritic cells, it may have similar effects on macrophages. To address this issue, we studied the effect of RANKL on various functions of macrophages using mouse bone marrow derived macrophages. RANKL enhanced the survival of macrophages and up-regulated the expression of CD86. RANKL-treated macrophages showed increased allogeneic T cell activation and phagocytic activity compared to control cells. In addition, RANKL increased the expression of TNFα, MCP-1, and IL-6 but not of IL-10, IL-12, IFN-γ, and iNOS. Collectively, RANKL augmented the activity of macrophages especially as antigen presenting cells, suggesting its new role in immune regulation.

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Section: Proinflammatory Cytokines and Inosmentioning

confidence: 64%

Receptor activator of NF-κB ligand enhances the activity of macrophages as antigen presenting cells

Park

Park²,

Shin³

et al. 2005

Exp Mol Med

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“…There are evidences that interaction between B-cell and T-cell may regulate B-cell production of cytokines involved in bone metabolism. In fact, B-cells suppress osteoclastogenesis if stimulated with Th1 cytokines while induce osteoclastogenesis when activated by Th2 cytokines [87].…”

Section: The Role Of B-cells In Osteoclastogenesismentioning

confidence: 99%

Osteoclastogenesis and arthritis

et al. 2010

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There is emerging interest for osteoclasts as key players in the erosive and inflammatory events leading to joint destruction in chronic arthritis. In fact, chronic inflammatory joint diseases such as psoriatic arthritis and rheumatoid arthritis are often characterized by destruction of juxta-articular bone and erosions due to the elevated activity of osteoclasts, which are involved in bone resorption. The main step in inflammatory bone erosion is an imbalance between bone resorption and bone formation: osteoclast formation is enhanced by proinflammatory cytokines such as TNF-α, IL-1β, and IL-17 and is not balanced by increased activity of bone-forming osteoblasts. T-cells, stromal cells, and synoviocytes enhance osteoclast formation via expression of RANKL and, under pathologic conditions, of proinflammatory cytokines. In rheumatoid arthritis, accumulation of osteoclasts in synovial tissues and their activation associated with osteoclastogenic cytokines and chemokines at cartilage erosion sites suggest that they could be usefully selected as therapeutic target. In particular, in consideration of the primary role of RANKL and TNF-α in osteoclastogenesis, the control of the production of RANKL and the inhibition of TNF-α represent important strategies for reducing bone damage in this disease.

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“…IL10 is a powerful TH2-cell cytokine produced by lymphoid cells that exerts its function by inhibiting macrophage/monocyte and T-cell lymphocyte replication and secretion of inflammatory cytokines (Redpath et al, 2001;Choi et al, 2003). Two SNPs in the promoter region, IL10 -1082 A G and -592 A C, are particularly interesting, because several previous reports have demonstrated quantitative differences in IL10 transcription and/or expression mediated by alternative alleles or haplotypes.…”

Section: Introductionmentioning

confidence: 99%