Clavicular cortical hyperostosis: new autoinflammatory entity or part of the juvenile spondyloarthropathies clinical picture?

Lamot, Lovro; Bukovac, Lana Tambić; Borovečki, Fran; Vlahoviček, Kristian; Sumić, Sara; Gotovac, Kristina; Bingula, Filip; Harjaček, Miroslav

doi:10.1186/1546-0096-9-s1-p299

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“…These include STAT3 downregulation, B-cell activation, apoptosis, and MAP kinase with upregulated TRPM3/7 Ca ++ channels, and the most interestingly, genes closely linked to autoinflammatory diseases PTPN12 and MEFV. Interestingly, stimulation of TRPM3/7 Ca ++ channels can provide a second signal for NLRP3 inflammasome activation suggesting that CCH might be indeed an early autoinflammatory presentation of jSpA [manuscript in preparation, (177)].…”

Section: Putting It All Togethermentioning

confidence: 99%

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Harjaček

2021

Front. Med.

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Juvenile spondyloarthritis (jSpA) is a an umbrella term for heterogeneous group of related seronegative inflammatory disorders sharing common symptoms. Although it mainly affects children and adolescents, it often remains active during adulthood. Genetic and environmental factors are involved in its occurrence, although the exact underlying immunopathophysiology remains incompletely elucidated. Accumulated evidence suggests that, in affected patients, subclinical gut inflammation caused by intestinal dysbiosis, is pivotal to the future development of synovial–entheseal complex inflammation. While the predominant role of IL17/23 axis, TNF-α, and IL-7 in the pathophysiology of SpA, including jSpA, is firmly established, the role of the cytokine macrophage migration inhibitory factor (MIF) is generally overlooked. The purpose of this review is to discuss and emphasize the role of epigenetics, neuroendocrine pathways and the hypothalamic-pituitary (HPA) axis, and to propose a novel hypothesis of the role of decreased NLRP3 gene expression and possibly MIF in the early phases of jSpA development. The decreased NLRP3 gene expression in the latter, due to hypomethylation of promotor site, is (one of) the cause for inflammasome malfunction leading to gut dysbiosis observed in patients with early jSpA. In addition, we highlight the role of MIF in the complex innate, adaptive cellular and main effector cytokine network, Finally, since treatment of advanced bone pathology in SpA remains an unmet clinical need, I suggest possible new drug targets with the aim to ultimately improve treatment efficacy and long-term outcome of jSpA patients.

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Section: Putting It All Togethermentioning

confidence: 99%

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Harjaček

2021

Front. Med.

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Clavicular cortical hyperostosis: new autoinflammatory entity or part of the juvenile spondyloarthropathies clinical picture?

Cited by 1 publication

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Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The “Out of the Box” View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF)

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