IL-17A inhibits osteoclast development by inducing the release of GM-CSF in osteoblast lineage cells

Balani, Deepak H.; Dolder, Silvia; Aeberli, Daniel; Kamgang, Richard; Hofstetter, Willy; Seitz, Michael

doi:10.1016/j.bone.2012.02.260

Cited by 2 publications

(2 citation statements)

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“…GM-CSF promotes joint damage by recruiting granulocyte and macrophage precursors from activated bone marrow adjacent to synovial joints and causes the release of pro-inflammatory chemokines such as CCL17 (46). These processes, which are expanded in the synovial fluid of patients with axial SpA, led by GM-CSF, also induce the destruction of the cartilage and the resorption of the bone, inducing several matrix metalloproteinases and the osteoclast activating factor—RANKL (Receptor Activator of Nuclear Factor Kappa-B Ligand) (47, 48).…”

Section: Gm-csf: a Novel Target In Asmentioning

confidence: 99%

RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

et al. 2019

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Susceptibility to ankylosing spondylitis (AS) is polygenic with more than 100 genes identified to date. These include HLA-B27 and the aminopeptidases (ERAP1, ERAP2, and LNPEPS), which are involved in antigen processing and presentation to T-cells, and several genes (IL23R, IL6R, STAT3, JAK2, IL1R1/2, IL12B, and IL7R) involved in IL23 driven pathways of inflammation. AS is also strongly associated with polymorphisms in two transcription factors, RUNX3 and T-bet (encoded by TBX21), which are important in T-cell development and function. The influence of these genes on the pathogenesis of AS and their potential for identifying drug targets is discussed here.

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Section: Gm-csf: a Novel Target In Asmentioning

confidence: 99%

RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

et al. 2019

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“…In addition, GM-CSF causes the release of pro-inflammatory chemokines such as CCL17 [ 46 ]. GM-CSF also facilitates cartilage destruction and bone resorption by the induction of matrix metalloproteinases [ 47 ] and the osteoclast activating factor RANKL [ 48 , 49 ]. Moreover, GM-CSF has been shown to be responsible for arthritic pain in mice independently of its pro-inflammatory characteristics and GM-CSF receptors have been shown to be expressed on nerve endings [ 50 , 51 ].…”

Section: Gm-csf As a Novel Target In Spondyloarthritismentioning

confidence: 99%

Novel Therapeutic Targets in Axial Spondyloarthritis

Worth

Bowness

Al-Mossawi

2018

Curr Treat Options in Rheum

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Purpose of reviewAxial spondyloarthritis remains an area of significant unmet clinical need with only two immune pathways currently targeted by licenced therapies compared to other immune-mediated inflammatory joint disorders such as rheumatoid arthritis where a multitude of therapeutic options are available. This review will look at emerging therapeutic targets in axial spondyloarthritis beyond the neutralisation of IL-17A and TNF by monoclonal antibodies.Recent findingsSeveral promising targets are in various stages of pre-clinical and clinical development in axial spondyloarthritis. These include small molecule approaches to target transcription factors, epigenetic modification and intracellular modulation of cytokine signalling by kinase inhibition. GM-CSF has also emerged as a potential driver of inflammation.SummaryA number of novel and promising therapeutic options are in various stages of development in axial spondyloarthritis. The Janus kinase inhibitors have shown great promise in other immune-mediated inflammatory disorders and will be an exciting addition to the axial spondyloarthritis field as the first oral disease-modifying agents. GM-CSF blockade also shows great promise since antibodies for neutralising this cytokine are safe in patients and have shown efficacy in other immune-mediated inflammatory diseases.

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IL-17A inhibits osteoclast development by inducing the release of GM-CSF in osteoblast lineage cells

Cited by 2 publications

References 0 publications

RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

RUNX3 and T-Bet in Immunopathogenesis of Ankylosing Spondylitis—Novel Targets for Therapy?

Novel Therapeutic Targets in Axial Spondyloarthritis

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