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  • 1
    Online Resource
    Online Resource
    Effectiveness of Soluble CTLA-4-Fc in the Inhibition of Bone Marrow T-Cell Activation in Context of Indoleamine 2.3-Dioxygenase (IDO) and CD4+Foxp3+ Treg Induction
    Informa UK Limited ; 2022
    In:  Journal of Inflammation Research Vol. Volume 15 ( 2022-12), p. 6813-6829
    Details
    In: Journal of Inflammation Research, Informa UK Limited, Vol. Volume 15 ( 2022-12), p. 6813-6829
    Type of Medium: Online Resource
    ISSN: 1178-7031
    URL: Article
    DOI: 10.2147/JIR.S359775
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2494878-0
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  • 2
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    Comprehensive microRNA and transcriptomic profiling of rheumatoid arthritis monocytes: role of microRNA-146b in pro-inflammatory progression
    Oxford University Press (OUP) ; 2021
    In:  Rheumatology Vol. 60, No. 11 ( 2021-11-03), p. 5424-5435
    Details
    In: Rheumatology, Oxford University Press (OUP), Vol. 60, No. 11 ( 2021-11-03), p. 5424-5435
    Abstract: To explore global miRNA and transcriptomic profiling of monocytes from RA patients compared with healthy controls in order to predict which aberrantly expressed miRNA can negatively modulate inflammatory molecules. Methods Using next-generation sequencing, we have performed simultaneous global analysis of miRNA (miRNA-seq) and transcriptome (RNA-seq) of monocytes from RA patients and healthy controls. Global analysis of miRNA of SSc monocytes was also performed. Following differential analysis and negative correlation, miRNA–RNA pairs were selected. Results We found that 20 specific miRNA candidates are predicted to silence inflammatory mediators, out of 191 significantly changed miRNAs in RA monocytes. Based on the highest scoring in terms of negative correlation (r = −0.97, P = 1.75e–07, false discovery rate = 0.04) and the number of seeds in miRNA responsible for negative regulation, we selected miRNA-146b and its target gene anti-inflammatory retinoic acid receptor alpha (RARA). Similarly to next-generation sequencing, qPCR analysis also confirmed negative correlation between miRNA-146b and RARA expression (r = −0.45, P = 0.04). Additionally, miRNA-146b expression in RA monocytes significantly correlated with clinical parameters including DAS28 for RA with CRP (DAS28-CRP) and ESR (DAS28-ESR), whereas overexpression of miRNA-146b was able to functionally reduce RARA expression in the human monocytic cell line THP-1. Finally, circulating miRNA-146b expression in sera and SFs was significantly elevated in RA patients. Conclusions Overall, in this study we have identified a new miRNA-146b candidate that is predicted to negatively regulate the anti-inflammatory RARA transcript, whereas circulating miRNA-146b level can be used as a biomarker predicting pro-inflammatory RA progression and disease activity.
    Type of Medium: Online Resource
    ISSN: 1462-0324 , 1462-0332
    URL: Article
    DOI: 10.1093/rheumatology/keab407
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 1474143-X
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  • 3
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    Image_5.tif
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-10-31)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-10-31)
    Abstract: Previous studies have shown a reduction in the effectiveness of primary COVID-19 vaccination in patients with rheumatic diseases. However, limited data is available regarding the effectiveness of the COVID-19 vaccine booster dose, especially on cellular response. The study aimed to assess the humoral and cellular immunogenicity of a booster dose in patients with inflammatory arthritis (IA). Patients and methods 49 IA and 47 age and sex-matched healthy controls (HC) were included in a prospective cohort study. Both groups completed primary COVID-19 vaccination and after more than 180 days received a BNT162b2 booster shot. Humoral responses (level of IgG antibodies) and cellular responses (IFN-γ production) were assessed before and after 4 weeks from the booster dose of the vaccine. Results After the booster dose, all participants showed an increased humoral response, although significantly reduced antibody levels were observed in IA patients compared to HC (p=0.004). The cellular response was significantly lower both before (p & lt;0.001) and after (p & lt;0.001) the booster dose in IA patients as compared to HC. Among the immunomodulatory drugs, only biological and targeted synthetic drugs lowered the humoral response after booster vaccination. However, the cellular response was decreased after all immunomodulatory drugs except IL-17 inhibitors and sulfasalazine. Conclusion Our data indicate that patients with rheumatic diseases present lower humoral and cellular responses after the COVID-19 booster vaccine in comparison to HC. This may translate into a recommendation for subsequent booster doses of the COVID-19 vaccine for rheumatic patients.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.1033804
    DOI: 10.3389/fimmu.2022.1033804.s001
    DOI: 10.3389/fimmu.2022.1033804.s002
    DOI: 10.3389/fimmu.2022.1033804.s003
    DOI: 10.3389/fimmu.2022.1033804.s004
    DOI: 10.3389/fimmu.2022.1033804.s005
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 4
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    Changes in MiRNA-5196 Expression as a Potential Biomarker of Anti-TNF-α Therapy in Rheumatoid Arthritis and Ankylosing Spondylitis Patients
    Springer Science and Business Media LLC ; 2018
    In:  Archivum Immunologiae et Therapiae Experimentalis Vol. 66, No. 5 ( 2018-10), p. 389-397
    Details
    In: Archivum Immunologiae et Therapiae Experimentalis, Springer Science and Business Media LLC, Vol. 66, No. 5 ( 2018-10), p. 389-397
    Type of Medium: Online Resource
    ISSN: 0004-069X , 1661-4917
    URL: Article
    DOI: 10.1007/s00005-018-0513-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2149971-8
    SSG: 12
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  • 5
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    The Kinetics of Humoral and Cellular Responses after the Booster Dose of COVID-19 Vaccine in Inflammatory Arthritis Patients
    MDPI AG ; 2023
    In:  Viruses Vol. 15, No. 3 ( 2023-02-24), p. 620-
    Details
    In: Viruses, MDPI AG, Vol. 15, No. 3 ( 2023-02-24), p. 620-
    Abstract: Impaired immunogenicity of COVID-19 vaccinations in inflammatory arthritis (IA) patients results in diminished immunity. However, optimal booster vaccination regimens are still unknown. Therefore, this study aimed to assess the kinetics of humoral and cellular responses in IA patients after the COVID-19 booster. In 29 IA patients and 16 healthy controls (HC), humoral responses (level of IgG antibodies) and cellular responses (IFN-γ production) were assessed before (T0), after 4 weeks (T1), and after more than 6 months (T2) from the booster vaccination with BNT162b2. IA patients, but not HC, showed lower anti-S-IgG concentration and IGRA fold change at T2 compared to T1 (p = 0.026 and p = 0.031). Furthermore, in IA patients the level of cellular response at T2 returned to the pre-booster level (T0). All immunomodulatory drugs, except IL-6 and IL-17 inhibitors for the humoral and IL-17 inhibitors for the cellular response, impaired the immunogenicity of the booster dose at T2. Our study showed impaired kinetics of both humoral and cellular responses after the booster dose of the COVID-19 vaccine in IA patients, which, in the case of cellular response, did not allow the vaccination effect to be maintained for more than 6 months. Repetitive vaccination with subsequent booster doses seems to be necessary for IA patients.
    Type of Medium: Online Resource
    ISSN: 1999-4915
    URL: Article
    DOI: 10.3390/v15030620
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2516098-9
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  • 6
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    Biologic Drugs for Rheumatoid Arthritis in the Context of Biosimilars, Genetics, Epigenetics and COVID-19 Treatment
    MDPI AG ; 2021
    In:  Cells Vol. 10, No. 2 ( 2021-02-04), p. 323-
    Details
    In: Cells, MDPI AG, Vol. 10, No. 2 ( 2021-02-04), p. 323-
    Abstract: Rheumatoid arthritis (RA) affects around 1.2% of the adult population. RA is one of the main reasons for work disability and premature retirement, thus substantially increasing social and economic burden. Biological disease-modifying antirheumatic drugs (bDMARDs) were shown to be an effective therapy especially in those rheumatoid arthritis (RA) patients, who did not adequately respond to conventional synthetic DMARD therapy. However, despite the proven efficacy, the high cost of the therapy resulted in limitation of the widespread use and unequal access to the care. The introduction of biosimilars, which are much cheaper relative to original drugs, may facilitate the achievement of the therapy by a much broader spectrum of patients. In this review we present the properties of original biologic agents based on cytokine-targeted (blockers of TNF, IL-6, IL-1, GM-CSF) and cell-targeted therapies (aimed to inhibit T cells and B cells properties) as well as biosimilars used in rheumatology. We also analyze the latest update of bDMARDs’ possible influence on DNA methylation, miRNA expression and histone modification in RA patients, what might be the important factors toward precise and personalized RA treatment. In addition, during the COVID-19 outbreak, we discuss the usage of biologicals in context of effective and safe COVID-19 treatment. Therefore, early diagnosing along with therapeutic intervention based on personalized drugs targeting disease-specific genes is still needed to relieve symptoms and to improve the quality of life of RA patients.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells10020323
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2661518-6
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  • 7
    Online Resource
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    DNA Methylation as a Future Therapeutic and Diagnostic Target in Rheumatoid Arthritis
    MDPI AG ; 2019
    In:  Cells Vol. 8, No. 9 ( 2019-08-22), p. 953-
    Details
    In: Cells, MDPI AG, Vol. 8, No. 9 ( 2019-08-22), p. 953-
    Abstract: Rheumatoid arthritis (RA) is a long-term autoimmune disease of unknown etiology that leads to progressive joint destruction and ultimately to disability. RA affects as much as 1% of the population worldwide. To date, RA is not a curable disease, and the mechanisms responsible for RA development have not yet been well understood. The development of more effective treatments and improvements in the early diagnosis of RA is direly needed to increase patients’ functional capacity and their quality of life. As opposed to genetic mutation, epigenetic changes, such as DNA methylation, are reversible, making them good therapeutic candidates, modulating the immune response or aggressive synovial fibroblasts (FLS—fibroblast-like synoviocytes) activity when it is necessary. It has been suggested that DNA methylation might contribute to RA development, however, with insufficient and conflicting results. Besides, recent studies have shown that circulating cell-free methylated DNA (ccfDNA) in blood offers a very convenient, non-invasive, and repeatable “liquid biopsy”, thus providing a reliable template for assessing molecular markers of various diseases, including RA. Thus, epigenetic therapies controlling autoimmunity and systemic inflammation may find wider implications for the diagnosis and management of RA. In this review, we highlight current challenges associated with the treatment of RA and other autoimmune diseases and discuss how targeting DNA methylation may improve diagnostic, prognostic, and therapeutic approaches.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells8090953
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
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  • 8
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    The role of micro RNA ‐5196 in the pathogenesis of systemic sclerosis
    Wiley ; 2017
    In:  European Journal of Clinical Investigation Vol. 47, No. 8 ( 2017-08), p. 555-564
    Details
    In: European Journal of Clinical Investigation, Wiley, Vol. 47, No. 8 ( 2017-08), p. 555-564
    Abstract: Systemic sclerosis ( SS c) is a chronic autoimmune disease characterised by tissue fibrosis and immune abnormalities. Recent evidence suggests that activated circulating monocytes from patients with SS c play an important role in early stages of SS c pathogenesis due to enhanced expression of tissue inhibitor of metalloproteinases 1 ( TIMP ‐1), IL ‐8 and reactive oxygen species ( ROS ) induction. However, the exact factors that contribute to chronic inflammation and subsequently fibrosis progression are still unknown. Materials and methods The expression pattern of IL ‐8, TIMP ‐1, AP ‐1 transcription factor‐Fra2 and ROS induction in peripheral blood monocytes following DZN ep (histone methyltransferase inhibitor) and TLR 8 agonist stimulation was investigated. Exogenous micro RNA ‐5196, which is predicted to bind 3′ UTR of Fra2 gene, was delivered to reverse profibrotic phenotype in monocytes. Expression of circulating micro RNA ‐5196 was correlated with SS c parameters. Results DZN ep +  TLR 8 agonist stimulation enhanced profibrotic TIMP ‐1, IL ‐8 and ROS generation in HC and SS c monocytes. As opposed by the decrease of mi RNA ‐5196 and antioxidant SOD 1 expression in SS c monocytes. Exogenous delivery of micro RNA ‐5196 reduced Fra2 and TIMP ‐1 expression suggesting that it may be used as a potential modulator of fibrogenesis in SS c. Circulating micro RNA ‐5196 was significantly increased in SS c and positively correlated with CRP level but not with Rodnan skin score or ESR . Conclusions These results suggest that micro RNA ‐5196 can be used as a potential biomarker characterising SS c. Overall, this study may open new possibilities for the development of micro RNA ‐5196‐based diagnostics and therapy in early phases of SS c.
    Type of Medium: Online Resource
    ISSN: 0014-2972 , 1365-2362
    URL: Issue
    URL: Article
    DOI: 10.1111/eci.2017.47.issue-8
    DOI: 10.1111/eci.12776
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2004971-7
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  • 9
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    Global miRNA and mRNA expression profiles identify miRNA‐26a‐2‐3p‐dependent repression of IFN signature in systemic sclerosis human monocytes
    Wiley ; 2020
    In:  European Journal of Immunology Vol. 50, No. 7 ( 2020-07), p. 1057-1066
    Details
    In: European Journal of Immunology, Wiley, Vol. 50, No. 7 ( 2020-07), p. 1057-1066
    Abstract: Dysregulation in type I IFN and IFN‐stimulated genes (ISGs) induced by monocytes is one of the key features of systemic sclerosis (SSc) pathogenesis. Abnormalities in microRNA (miRNA) expression are related to excessive IFN production, however the role of miRNA remains largely elusive in SSc monocytes. This study explores global miRNA‐mRNA profiling of SSc monocytes and functional attenuation of IFN and ISGs by specific miRNAs. Global sequencing of mRNA (mRNA‐seq) and miRNA (miRNA‐seq) samples were performed simultaneously on healthy controls and SSc monocytes. Following computational analysis, selected miRNAs–mRNA candidates were validated, correlated with clinical parameters, and tested by functional assays. Transcriptomics data and qPCR analysis confirmed IFN signature in SSc but not in rheumatoid arthritis monocytes. Based on miRNA‐seq analysis, five miRNAs were selected for further validation. Only the expression patterns of miRNA‐26a‐2‐3p and miRNA‐485‐3p were confirmed and negatively correlated with clinical parameters. Exogenous delivery of miRNA‐26a‐2‐3p to TLR‐stimulated monocytic THP‐1 cells specifically inhibited ISGs but not inflammasome activity in functional assays. In conclusion, our miRNA–mRNA co‐sequencing and functional analysis identify miRNA‐26a‐2‐3p as a new candidate, which is predicated to negatively regulate ISGs. This implies that reduced expression of miRNA‐26a‐2‐3 may be involved in pathogenic IFN signature in SSc monocytes.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v50.7
    DOI: 10.1002/eji.201948428
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1491907-2
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  • 10
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    Small Molecule Inhibitors in the Treatment of Rheumatoid Arthritis and Beyond: Latest Updates and Potential Strategy for Fighting COVID-19
    MDPI AG ; 2020
    In:  Cells Vol. 9, No. 8 ( 2020-08-11), p. 1876-
    Details
    In: Cells, MDPI AG, Vol. 9, No. 8 ( 2020-08-11), p. 1876-
    Abstract: The development of biological disease-modifying antirheumatic drugs (bDMARDs) and target synthetic DMARDs (tsDMARDs), also known as small molecule inhibitors, represent a breakthrough in rheumatoid arthritis (RA) treatment. The tsDMARDs are a large family of small molecules targeting mostly the several types of kinases, which are essential in downstream signaling of pro-inflammatory molecules. This review highlights current challenges associated with the treatment of RA using small molecule inhibitors targeting intracellular JAKs/MAPKs/NF-κB/SYK-BTK signaling pathways. Indeed, we have provided the latest update on development of small molecule inhibitors, their clinical efficacy and safety as a strategy for RA treatment. On the other hand, we have highlighted the risk and adverse effects of tsDMARDs administration including, among others, infections and thromboembolism. Therefore, performance of blood tests or viral infection screening should be recommended before the tsDMARDs administration. Interestingly, recent events of SARS-CoV-2 outbreak have demonstrated the potential use of small molecule inhibitors not only in RA treatment, but also in fighting COVID-19 via blocking the viral entry, preventing of hyperimmune activation and reducing cytokine storm. Thus, small molecule inhibitors, targeting wide range of pro-inflammatory singling pathways, may find wider implications not only for the management of RA but also in the controlling of COVID-19.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells9081876
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2661518-6
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