Serum heat-shock protein-65 antibody levels are elevated but not associated with disease activity in patients with rheumatoid arthritis and ankylosing spondylitis

Ulusoy, Hasan; Akgol, Gurkan; Gulkesen, Arif; Kaya, Arzu; Kal, Gül Ayden; Kaman, Dilara; Tuncer, Türkan

doi:10.2147/oarrr.s162512

Cited by 3 publications

(6 citation statements)

References 34 publications

(48 reference statements)

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“…Previous studies confirmed that HSPs are immune system targets in AS. − HSPs and their synthetic peptides help develop potential immunotherapy for autoimmune diseases . Compared with healthy controls, AS patients showed higher serum level HPS-65 antibody (anti-HSP65) . In our study, we identified two HSP90 (HSP90AA1 and HSP90AB1) with both expression and phosphorylation differences in PBMCs between AS patients and healthy controls.…”

Section: Discussionsupporting

confidence: 59%

“…Increasing studies indicated that heat-shock proteins (HSPs) are indispensable in innate and adaptive immunities. 30 − 35 HSPs are known to awake the immune-regulatory systems and stimulate regulatory T cells that result in the secretion of IL10 and TGF-β. 30 Previous studies confirmed that HSPs are immune system targets in AS.…”

Section: Discussionmentioning

confidence: 99%

“…Target antigen determination is essential to understand the pathogenesis and develop new therapy strategies in autoimmune diseases. Increasing studies indicated that heat-shock proteins (HSPs) are indispensable in innate and adaptive immunities. − HSPs are known to awake the immune-regulatory systems and stimulate regulatory T cells that result in the secretion of IL10 and TGF-β . Previous studies confirmed that HSPs are immune system targets in AS. − HSPs and their synthetic peptides help develop potential immunotherapy for autoimmune diseases .…”

Section: Discussionmentioning

confidence: 99%

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Quantitative Proteomic Analyses To Reveal the Key Features of Proteins in New Onset Ankylosing Spondylitis Patients

Zhang

Zheng

et al. 2020

ACS Omega

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Ankylosing spondylitis (AS) is a chronic immune-mediated disease. Various immune cells play an essential role in the AS pathogenesis. However, the specific pathogenesis of AS has not been well understood. Proteomic profiles of peripheral blood mononuclear cells (PBMCs) were applied to reveal the specific pathogenesis of AS. Quantitative proteomic analyses were performed using liquid chromatography–tandem mass spectrometry (LC–MS/MS)-based methods to investigate the protein profiling of PBMCs from new-onset AS patients ( n = 9) and healthy controls ( n = 9). We identified 782 differentially expressed proteins (DEPs) and 527 differentially phosphorylated proteins (DPPs) between AS patients and healthy controls. The subcellular location of DEPs and DPPs showed that most of the DEPs were from the cytoplasm ( n = 296, 38%), were extracellular ( n = 141, 18%), and from the nucleus ( n = 114, 15%); most of the DPPs were from the cytoplasm ( n = 37, 34%), nucleus ( n = 35, 32%), and plasma membrane ( n = 10, 9%). We further identified 89 proteins with both expression and phosphorylation differences. The functional annotation of the 89 differentially expressed and phosphorylated proteins enriched in the antigen processing and presentation pathway. Four DEPs with six phosphorylated positions were found in the antigen processing and presentation pathway. The differentially expressed and phosphorylated proteins may be helpful to uncover the pathogenesis of AS. The six AS-specific proteins may serve as candidate markers for AS diagnosis and new treatment targets.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Quantitative Proteomic Analyses To Reveal the Key Features of Proteins in New Onset Ankylosing Spondylitis Patients

Zhang

Zheng

et al. 2020

ACS Omega

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“…In addition to these types of antibodies, traditionally associated with systemic autoimmune diseases, antibodies to the intracellular protein prefoldin subunit 5 (PFDN5) have also been found in a subgroup of AS patients [73,87]. PFDN5 is a chaperone protein that is involved in stabilizing polypeptides and protecting cells from aggregated protein-induced cell death [106].…”

Section: Autoantibodies Reactive To Intracellular Antigensmentioning

confidence: 99%

“…Another example of the involvement of molecular mimicry in AS pathogenesis is the heat shock proteins on Mycobacterium that cross-react with self HSPs. In AS patients, but also in patients with other autoimmune diseases, such as RA and pSS, serum IgG antibodies to Mycobacterium HSP65 are significantly elevated compared to controls [87,142]. These antibodies cross-react with human HSP65, but the functional consequences of these anti-HSP65 antibodies, as well as the anti-DPP antibodies for the initiation and/or perpetuation of AS, are not understood.…”

Section: Antibodies To Cross-reactive Microbial Antigensmentioning

confidence: 99%

B Cell Involvement in the Pathogenesis of Ankylosing Spondylitis

Wilbrink

Spoorenberg

Verstappen

et al. 2021

IJMS

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Extensive research into ankylosing spondylitis (AS) has suggested the major role of genetics, immune reactions, and the joint–gut axis in its etiology, although an ultimate consensus does not yet exist. The available evidence indicates that both autoinflammation and T-cell-mediated autoimmune processes are actively involved in the disease process of AS. So far, B cells have received relatively little attention in AS pathogenesis; this is largely due to a lack of conventional disease-defining autoantibodies. However, against prevailing dogma, there is a growing body of evidence suggestive of B cell involvement. This is illustrated by disturbances in circulating B cell populations and the formation of auto-reactive and non-autoreactive antibodies, along with B cell infiltrates within the axial skeleton of AS patients. Furthermore, the depletion of B cells, using rituximab, displayed beneficial results in a subgroup of patients with AS. This review provides an overview of our current knowledge of B cells in AS, and discusses their potential role in its pathogenesis. An overarching picture portrays increased B cell activation in AS, although it is unclear whether B cells directly affect pathogenesis, or are merely bystanders in the disease process.

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