Immunoregulatory Property of C-Type Lectin-Like Receptors in Fibrosing Interstitial Lung Diseases

Effendi, Wiwin Is; Nagano, Tatsuya; Hasan, Helmia; Yudhawati, Resti

doi:10.3390/ijms21103665

Cited by 9 publications

(4 citation statements)

References 113 publications

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“…Inhibition of renal fibrosis by suppressing MINCLE-induced inflammation can alleviate the progression of chronic kidney disease ( 68 ). By regulating the expression of macrophage colony-stimulating factor (M-CSF) to control fibrosis, C-type lectin-like receptors (CTLRs) play a significant role in interstitial lung disease ( 69 ).…”

Section: Introductionmentioning

confidence: 99%

Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis

Liu

Chen

2022

Front. Immunol.

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Fibrosis is defined as the abnormal and excessive deposition of extracellular matrix (ECM) components, which leads to tissue or organ dysfunction and failure. However, the pathological mechanisms underlying fibrosis remain unclear. The inflammatory response induced by tissue injury is closely associated with tissue fibrosis. Recently, an increasing number of studies have linked necroptosis to inflammation and fibrosis. Necroptosis is a type of preprogrammed death caused by death receptors, interferons, Toll-like receptors, intracellular RNA and DNA sensors, and other mediators. These activate receptor-interacting protein kinase (RIPK) 1, which recruits and phosphorylates RIPK3. RIPK3 then phosphorylates a mixed lineage kinase domain-like protein and causes its oligomerization, leading to rapid plasma membrane permeabilization, the release of cellular contents, and exposure of damage-associated molecular patterns (DAMPs). DAMPs, as inflammatory mediators, are involved in the loss of balance between extensive inflammation and tissue regeneration, leading to remodeling, the hallmark of fibrosis. In this review, we discuss the role of necroptotic DAMPs in tissue fibrosis and highlight the inflammatory responses induced by DAMPs in tissue ECM remodeling. By summarizing the existing literature on this topic, we underscore the gaps in the current research, providing a framework for future investigations into the relationship among necroptosis, DAMPs, and fibrosis, as well as a reference for later transformation into clinical treatment.

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Section: Introductionmentioning

confidence: 99%

Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis

Liu

Chen

2022

Front. Immunol.

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“…Besides roles in cell adhesion and cell-cell signaling, CLEC12A is expressed in alveolar macrophages and has been suggested to be involved in the pathogenicity of fibrosing lung disease. 17 Virtually all genes upregulated in RA-ILD vs RA without ILD in our investigation are involved in the pathogenesis of fibrosis.…”

Section: Discussionmentioning

confidence: 77%

A Call for Gene Expression Analysis in Whole Blood of Patients With Rheumatoid Arthritis (RA) as a Biomarker for RA-Associated Interstitial Lung Disease

Wierczeiko,

Linke,

Friedrich

et al. 2023

J Rheumatol

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ObjectiveRheumatoid arthritis interstitial lung disease (RA-ILD) is one of the most common and prognostic organ manifestations of rheumatoid arthritis. Therefore, to allow an effective treatment, it is of crucial importance to diagnose RA-ILD at the earliest possible stage. So far, the gold standard of early detection has been an HR-CT of the lungs. This procedure involves considerable radiation exposure for the patient and is, therefore, unsuitable as a routine screening measure for ethical reasons. Here, we propose the analysis of characteristic gene expression patterns as biomarker to aid in the early detection and initiation of appropriate (possibly antifibrotic) therapy.MethodsTo investigate unique molecular patterns of RA-ILD, whole blood samples were taken from 12 female patients suffering from RA-ILD (n=7) or RA (n=5). The RNA was extracted, sequenced by RNA-seq, and analyzed for characteristic differences in the gene expression patterns between RA-ILD and RA patients.ResultsThe differential gene expression analysis revealed nine significantly upregulated genes in RA-ILD compared to RA without ILD: ARG1, TYMS, SORT1, MKI67, OLFM4, BIRC5, MS4A4A, CLEC12A, RNA LINC02967.ConclusionAll gene products of these genes (except for LINC02967) are known from the literature to be involved in the pathogenesis of fibrosis. Furthermore, for some, a contribution to the development of pulmonary fibrosis has even been demonstrated in experimental studies. Therefore, the results presented here provide an encouraging perspective for using specific gene expression patterns as biomarkers for the early detection and differential diagnosis of RA-ILD as a routine screening test.

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“…TD139 treatment also inhibits pro-tumorigenic effects in thyroid cancer cells by attenuating AKT phosphorylation and reducing the expression of MMP2 and β-catenin, which leads to the suppression of anoikis resistance, motility and invasion (336). The β-glycan receptor dectin-1 is a potential biomarker of lung fibrosis (337). Dectin-1 is highly expressed in bone-marrowderived myeloid cells, including monocytes, macrophages, and neutrophils (338).…”

Section: Galectin-3mentioning

confidence: 99%

Galectin functions in cancer-associated inflammation and thrombosis

Kruk

Braun²,

Cosset³

et al. 2023

Front. Cardiovasc. Med.

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Galectins are carbohydrate-binding proteins that regulate many cellular functions including proliferation, adhesion, migration, and phagocytosis. Increasing experimental and clinical evidence indicates that galectins influence many steps of cancer development by inducing the recruitment of immune cells to the inflammatory sites and modulating the effector function of neutrophils, monocytes, and lymphocytes. Recent studies described that different isoforms of galectins can induce platelet adhesion, aggregation, and granule release through the interaction with platelet-specific glycoproteins and integrins. Patients with cancer and/or deep-venous thrombosis have increased levels of galectins in the vasculature, suggesting that these proteins could be important contributors to cancer-associated inflammation and thrombosis. In this review, we summarize the pathological role of galectins in inflammatory and thrombotic events, influencing tumor progression and metastasis. We also discuss the potential of anti-cancer therapies targeting galectins in the pathological context of cancer-associated inflammation and thrombosis.

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Immunoregulatory Property of C-Type Lectin-Like Receptors in Fibrosing Interstitial Lung Diseases

Cited by 9 publications

References 113 publications

Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis

Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis

A Call for Gene Expression Analysis in Whole Blood of Patients With Rheumatoid Arthritis (RA) as a Biomarker for RA-Associated Interstitial Lung Disease

Galectin functions in cancer-associated inflammation and thrombosis

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