C1q/TNF-related protein 6 is a new pattern recognition molecule that modulates complement activity

Kirketerp-Møller, Nikolaj; Bayarri‐Olmos, Rafael; Sørensen, Camilla Adler; Krogfelt, Karen A.; Garred, Peter

doi:10.1016/j.molimm.2018.06.125

Cited by 2 publications

(2 citation statements)

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“…The study also demonstrated that the urinary sC5b-9 levels normalized after treatment with eculizumab, highlighting its role in assessing treatment response. Interestingly, the urinary excretion of sC5b-9 did not correlate with the plasma levels of sC5b-9, confirming that local complement activation is associated with kidney disease activity in C3 glomerulopathy ( 87 ). These findings are similar to the preliminary findings of a clinical trial studying the effect of an unknown complement blocking agent on plasma and urinary Ba and sC5b-9 levels.…”

Section: Kidney Disease Due To Alternative Complement Pathway Activationmentioning

confidence: 90%

Urinary complement biomarkers in immune-mediated kidney diseases

Kesarwani,

Bukhari,

Kahlenberg

et al. 2024

Front. Immunol.

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The complement system, an important part of the innate system, is known to play a central role in many immune mediated kidney diseases. All parts of the complement system including the classical, alternative, and mannose-binding lectin pathways have been implicated in complement-mediated kidney injury. Although complement components are thought to be mainly synthesized in the liver and activated in the circulation, emerging data suggest that complement is synthesized and activated inside the kidney leading to direct injury. Urinary complement biomarkers are likely a better reflection of inflammation within the kidneys as compared to traditional serum complement biomarkers which may be influenced by systemic inflammation. In addition, urinary complement biomarkers have the advantage of being non-invasive and easily accessible. With the rise of therapies targeting the complement pathways, there is a critical need to better understand the role of complement in kidney diseases and to develop reliable and non-invasive biomarkers to assess disease activity, predict treatment response and guide therapeutic interventions. In this review, we summarized the current knowledge on urinary complement biomarkers of kidney diseases due to immune complex deposition (lupus nephritis, primary membranous nephropathy, IgA nephropathy) and due to activation of the alternative pathway (C3 glomerulopathy, thrombotic microangiography, ANCA-associated vasculitis). We also address the limitations of current research and propose future directions for the discovery of urinary complement biomarkers.

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Section: Kidney Disease Due To Alternative Complement Pathway Activationmentioning

confidence: 90%

Urinary complement biomarkers in immune-mediated kidney diseases

Kesarwani,

Bukhari,

Kahlenberg

et al. 2024

Front. Immunol.

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“…C1QTNF6 is an important member of the C1QTNF family. It was originally found to exert inflammatoryregulating effects in several diseases (Kirketerp-Moller, Bayarri-Olmos, Krogfelt, & Garred, 2020). C1QTNF6 is crucially involved in alleviating OGD-induced inflammatory molecules, including TNF-α, IL-1β, IL-6, and IL-10, in PC12 cells.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA H19 promotes leukocyte inﬂammation in ischaemic stroke by targeting the miR-29b/C1QTNF6 axis

Li,

Ma,

Zhao

et al. 2024

Preprint

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Background and Purpose Inflammatory processes induced by leukocytes are crucially involved in the pathophysiology of acute ischemic stroke. This study aimed to elucidate the inflammatory mechanism of long non-coding RNA (lncRNA) H19-mediated regulation of C1QTNF6 by sponging miR-29b in leukocytes during ischemic stroke. Experimental Approach H19 and miR-29b expression in leukocytes of patients with ischemic stroke and middle cerebral artery occlusion rats was measured through real-time PCR. Moreover, we performed in vivo and in vitro experiments to determine the impact of H19 and miR-29b on C1QTNF6 expression in leukocytes after ischemic injury. Key Results There was H19 and C1QTNF6 upregulation, as well as miR-29b downregulation, in neutrophils of patients with stroke. Moreover, miR-29b could bind C1QTNF6 mRNA to repress its expression while H19 could sponge miR-29b to maintain C1QTNF6 expression. Moreover, C1QTNF6 overexpression promoted the release of IL-1β and TNF-α in leukocytes and further exacerbates blood-brain barrier disruption. Conclusion and Implications Our findings confirm the inflammation-modulatory effect of the H19/miR-29b/C1QTNF6 axis on cerebral ischemic injury.

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C1q/TNF-related protein 6 is a new pattern recognition molecule that modulates complement activity

Cited by 2 publications

References 0 publications

Urinary complement biomarkers in immune-mediated kidney diseases

Urinary complement biomarkers in immune-mediated kidney diseases

Long noncoding RNA H19 promotes leukocyte inﬂammation in ischaemic stroke by targeting the miR-29b/C1QTNF6 axis

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