Serum anti-lysozyme is associated with disease activity of Behçet's disease

Park, Jin Su; Kang, Moon Gi; Ha, You Jung; Song, Jason Jungsik; Park, Yong Bum; Lee, Soo Kon; Lee, Sang Won

doi:10.1111/1756-185x.12832

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…We found that antimicrobial proteins lysozyme and lactoferrin can, like LL37, promote TLR9 activation of B cells in complex with DNA. Interestingly, pathogenic anti-lysozyme abs have been described in Behçet's disease (28), whereas antilactoferrin abs have been described in autoimmune hepatitis (29), suggesting a mechanism of dual TLR9/BCR engagement for autoantibody induction that is similar to that described for LL37.…”

Section: Discussionmentioning

confidence: 92%

Netting Neutrophils Activate Autoreactive B Cells in Lupus

Gestermann

Domizio

Lande³

et al. 2018

The Journal of Immunology

137

124

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Lupus erythematosus (LE) patients develop autoantibodies that form circulating immune complexes (ICs) with extracellular self-nucleic acids. These ICs are deposited into peripheral tissues, where they trigger detrimental organ inflammation. Recent evidence suggests that ICs contain LL37-DNA complexes derived from neutrophil extracellular traps (NETs) and that LE patients develop pathogenic autoantibodies against these structures, including Abs to LL37. However, the mechanism that leads to the generation of these Abs is unknown. In this study, we show that NETs directly trigger Ab production by human memory B cells. This occurs via LL37-DNA complexes present in NETs, which have the unique ability to gain access to endosomal compartments of B cells and to trigger TLR9 activation. In LE patients, NET-derived LL37-DNA complexes trigger polyclonal B cell activation via TLR9, but also specifically expand self-reactive memory B cells producing anti-LL37 Abs in an Ag-dependent manner. These findings suggest a unique link between neutrophils and B cells in which NETs trigger a concerted activation of TLR9 and BCR leading to anti-NET autoantibody production in lupus.

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Section: Discussionmentioning

confidence: 92%

Netting Neutrophils Activate Autoreactive B Cells in Lupus

Gestermann

Domizio

Lande³

et al. 2018

The Journal of Immunology

137

124

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“…[ 4 ] Because of the lack of a universally recognized pathognomonic laboratory test, the diagnosis relies heavily on mucocutaneous manifestations and other clinical findings. [ 5 ] In order to diagnose and monitor disease activity in BD, many cytokines and biomarkers have been identified such as antilysozyme, [ 6 ] serum endocan, [ 7 ] serum growth differentiation factor 15 (GDF-15), [ 8 ] serum alpha 1-acid glycoprotein, [ 9 ] interleukin (IL)-8, [ 10 ] erythrocyte sedimentation rate (ESR), [ 11 ] and high-sensitivity C-reactive protein (hs-CRP). [ 12 ] However, they are not routinely used in clinical practice as they are not simple or easily derived.…”

Section: Introductionmentioning

confidence: 99%

Serum PLR and LMR in Behçet's disease

Jiang¹,

Zang

Li³

2017

Medicine

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The aim of this study is to determine platelet to lymphocyte ratio (PLR) and lymphocytes to monocytes ratio (LMR) levels in Behçet's disease (BD) and to investigate their relationships with disease activity.Hematological and inflammatory parameters including high-sensitivity C-reactive proteins (hs-CRP), erythrocyte sedimentation rate (ESR), PLR, and LMR were examined in BD and healthy controls.Data from 140 patients with BD (108 with active and 32 with inactive disease) and 107 controls were enrolled. PLR (153.21 ± 65.44, 106.20 ± 28.91, P <.001, respectively) was remarkably higher, whereas LMR (5.37 ± 5.47, 8.95 ± 5.84, P <.001, respectively) was significantly lower in BD than in controls. Active BD patients had significantly higher PLR (159.20 vs 131.14, P = .037), ESR (38.30 vs 24.55, P = .017), and hs-CRP (30.20 vs 17.21, P = .027) than those with inactive BD. However, no significant difference in LMR was found between the groups. Moreover, PLR was positively correlated with BDCAF (r = 0.193, P <.05), hs-CRP (r = 0.402, P <.01), and ESR (r = 0.284, P <.01), whereas LMR was negatively correlated with BDCAF (r = –0.175, P <.05), hs-CPR (r = –0.263, P <.01), and ESR (r = –0.175, P <.05). Additionally, both PLR and LMR were shown to be independent factors for BD by multivariate logistic regression analysis. Furthermore, a PLR level of 124.63 was determined as the best cut-off value by ROC analysis (sensitivity 64.3%, specificity 78.0%, and the area under the ROC curve 0. 753).PLR was elevated in active BD as compared to inactive BD. PLR may be a reliable, cost-effective, and novel potential parameter to help evaluate disease activity in BD.

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“…Lysozyme-C increased 13.72-fold in IgAV. Lysozymes were found in myelocyte/ macrophage cells within capillary loops and arterial walls in acute necrotizing vasculitis and have been considered as inflammatory markers [43,44].…”

Section: Discussionmentioning

confidence: 99%

Plasma Proteomic Analysis Reveals the Potential Role of Lectin and Alternative Complement Pathways in IgA Vasculitis Pathogenesis

et al. 2023

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Background: IgA vasculitis (IgAV) is the most common form of childhood vasculitis. A better understanding of its pathophysiology is required to identify new potential biomarkers and treatment targets. Objective: to assess the underlying molecular mechanisms in the pathogenesis of IgAV using an untargeted proteomics approach. Methods: Thirty-seven IgAV patients and five healthy controls were enrolled. Plasma samples were collected on the day of diagnosis before any treatment was initiated. We used nano-liquid chromatography–tandem mass spectrometry (nLC–MS/MS) to investigate the alterations in plasma proteomic profiles. For the bioinformatics analyses, databases including Uniprot, PANTHER, KEGG, Reactome, Cytoscape, and IntAct were used. Results: Among the 418 proteins identified in the nLC–MS/MS analysis, 20 had significantly different expressions in IgAV patients. Among them, 15 were upregulated and 5 were downregulated. According to the KEGG pathway and function classification analysis, complement and coagulation cascades were the most enriched pathways. GO analyses showed that the differentially expressed proteins were mainly involved in defense/immunity proteins and the metabolite interconversion enzyme family. We also investigated molecular interactions in the identified 20 proteins of IgAV patients. We extracted 493 interactions from the IntAct database for the 20 proteins and used Cytoscape for the network analyses. Conclusion: Our results clearly suggest the role of the lectin and alternate complement pathways in IgAV. The proteins defined in the pathways of cell adhesion may serve as biomarkers. Further functional studies may lead the way to better understanding of the disease and new therapeutic options for IgAV treatment.

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Serum anti-lysozyme is associated with disease activity of Behçet's disease

Cited by 8 publications

References 22 publications

Netting Neutrophils Activate Autoreactive B Cells in Lupus

Netting Neutrophils Activate Autoreactive B Cells in Lupus

Serum PLR and LMR in Behçet's disease

Plasma Proteomic Analysis Reveals the Potential Role of Lectin and Alternative Complement Pathways in IgA Vasculitis Pathogenesis

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