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Article ; Online: Cytokines as Biomarkers in Systemic Lupus Erythematosus

Helena Idborg / Vilija Oke

International Journal of Molecular Sciences, Vol 22, Iss 11327, p

Value for Diagnosis and Drug Therapy

2021 Volume 11327

Abstract: Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease. The disease is characterized by activation and dysregulation of both the innate and the adaptive immune systems. The autoimmune response targets self-molecules including cell nuclei, ... ...

Abstract	Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease. The disease is characterized by activation and dysregulation of both the innate and the adaptive immune systems. The autoimmune response targets self-molecules including cell nuclei, double stranded DNA and other intra and extracellular structures. Multiple susceptibility genes within the immune system have been identified, as well as disturbances in different immune pathways. SLE may affect different organs and organ systems, and organ involvement is diverse among individuals. A universal understanding of pathophysiological mechanism of the disease, as well as directed therapies, are still missing. Cytokines are immunomodulating molecules produced by cells of the immune system. Interferons (IFNs) are a broad group of cytokines, primarily produced by the innate immune system. The IFN system has been observed to be dysregulated in SLE, and therefore IFNs have been extensively studied with a hope to understand the disease mechanisms and identify novel targeted therapies. In several autoimmune diseases identification and subsequent blockade of specific cytokines has led to successful therapies, for example tumor necrosis factor-alpha (TNF-α) inhibition in rheumatoid arthritis. Authors of this review have sought corresponding developments in SLE. In the current review, we cover the actual knowledge on IFNs and other studied cytokines as biomarkers and treatment targets in SLE.
Keywords	lupus ; systemic lupus erythematosus ; SLE ; biomarkers ; cytokines ; interferons ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Cytokines as Biomarkers in Systemic Lupus Erythematosus: Value for Diagnosis and Drug Therapy.

Idborg, Helena / Oke, Vilija

International journal of molecular sciences

2021 Volume 22, Issue 21

Abstract	Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease. The disease is characterized by activation and dysregulation of both the innate and the adaptive immune systems. The autoimmune response targets self-molecules including cell nuclei, double stranded DNA and other intra and extracellular structures. Multiple susceptibility genes within the immune system have been identified, as well as disturbances in different immune pathways. SLE may affect different organs and organ systems, and organ involvement is diverse among individuals. A universal understanding of pathophysiological mechanism of the disease, as well as directed therapies, are still missing. Cytokines are immunomodulating molecules produced by cells of the immune system. Interferons (IFNs) are a broad group of cytokines, primarily produced by the innate immune system. The IFN system has been observed to be dysregulated in SLE, and therefore IFNs have been extensively studied with a hope to understand the disease mechanisms and identify novel targeted therapies. In several autoimmune diseases identification and subsequent blockade of specific cytokines has led to successful therapies, for example tumor necrosis factor-alpha (TNF-α) inhibition in rheumatoid arthritis. Authors of this review have sought corresponding developments in SLE. In the current review, we cover the actual knowledge on IFNs and other studied cytokines as biomarkers and treatment targets in SLE.
MeSH term(s)	Animals ; B-Cell Activating Factor/immunology ; B-Cell Activating Factor/metabolism ; Biomarkers ; Cytokines/immunology ; Cytokines/metabolism ; Humans ; Interferons/immunology ; Interferons/metabolism ; Interleukins/immunology ; Interleukins/metabolism ; Lupus Erythematosus, Systemic/diagnosis ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 13/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 13/metabolism ; Tumor Necrosis Factor-alpha/immunology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	B-Cell Activating Factor ; Biomarkers ; Cytokines ; Interleukins ; Tumor Necrosis Factor Ligand Superfamily Member 13 ; Tumor Necrosis Factor-alpha ; Interferons (9008-11-1)
Language	English
Publishing date	2021-10-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222111327
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Article ; Online: Anti-histone and anti-nucleosome rather than anti-dsDNA antibodies associate with IFN-induced biomarkers in Sudanese and Swedish Systemic Lupus Erythematosus patients.

Elbagir, Sahwa / Mohammed, NasrEldeen A / Oke, Vilija / Larsson, Anders / Nilsson, Jan / Elshafie, Amir / Elagib, Elnour M / Nur, Musa A M / Gunnarsson, Iva / Svenungsson, Elisabet / Rönnelid, Johan

Rheumatology (Oxford, England)

2024

Abstract: Objectives: In SLE, anti-dsDNA can co-occur with autoantibodies against other chromatin components, like histones and nucleosomes. These antibodies induce type-1 interferon production, a hallmark of SLE. We measured antinuclear antibody (ANA) sub- ... ...

Abstract	Objectives: In SLE, anti-dsDNA can co-occur with autoantibodies against other chromatin components, like histones and nucleosomes. These antibodies induce type-1 interferon production, a hallmark of SLE. We measured antinuclear antibody (ANA) sub-specificities and investigated their associations to inflammatory biomarkers including interferon-regulated chemokines. Methods: We included 93 Sudanese and 480 Swedish SLE patients and matched controls (N = 104 + 192). Autoantibodies targeting ANA-subspecificites: dsDNA, Sm, Sm/U1RNPcomplex, U1RNP, SSA/Ro52, SSA/Ro60, SSB/La, ribosomal P, PCNA and histones were quantified in all subjects, anti-nucleosome only in the Swedish patients, with a bead-based multiplex immunoassay. Levels of 72 plasma biomarkers were determined with Proximity Extension Assay technique or ELISA. Results: Among Sudanese patients, the investigated antibodies significantly associated with 9/72 biomarkers. Anti-histone antibodies showed the strongest positive correlations with MCP-3 and S100A12 as well as with interferon I-inducible factors MCP-1 and CXCL10. Anti-dsDNA antibodies associated with CXCL10 and S100A12, but in multivariate analyses, unlike anti-histone, associations lost significance.Among Swedish patients, MCP-1, CXCL10, SA100A12 also demonstrated stronger associations to anti-histone and anti-nucleosome antibodies, compared with anti-dsDNA and other ANA sub-specificities. In multiple regression models, anti-histone/nucleosome retained the strongest associations. When excluding anti-histone or anti-nucleosome positive patients, the associations between MCP-1/CXCL10 and anti-dsDNA were lost. In contrast, when excluding anti-dsDNA positive patients, associations with anti-histone and anti-nucleosome remained significant. Conclusion: In two cohorts of different ethnical origin, autoantibodies targeting chromatin correlate stronger with IFN-induced inflammatory biomarkers than anti-dsDNA or other ANA sub-specificities. Our results suggest that anti-histone/nucleosome autoantibodies may be main drivers of type-1 interferon activity in SLE.
Language	English
Publishing date	2024-03-09
Publishing country	England
Document type	Journal Article
ZDB-ID	1464822-2
ISSN	1462-0332 ; 1462-0324
ISSN (online)	1462-0332
ISSN	1462-0324
DOI	10.1093/rheumatology/keae134
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Article: Interleukin (IL) 16: a candidate urinary biomarker for proliferative lupus nephritis.

Häyry, Aliisa / Faustini, Francesca / Zickert, Agneta / Larsson, Anders / Niewold, Timothy B / Svenungsson, Elisabet / Oke, Vilija / Gunnarsson, Iva

Lupus science & medicine

2022 Volume 9, Issue 1

Abstract: Objective: Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE). The pathogenesis is incompletely understood and diagnostic biomarkers are scarce. We investigated interleukin (IL) 16 as a potential biomarker for LN in a ... ...

Abstract	Objective: Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE). The pathogenesis is incompletely understood and diagnostic biomarkers are scarce. We investigated interleukin (IL) 16 as a potential biomarker for LN in a well-characterised cohort of patients with SLE. Methods: We measured urinary (u-) and plasma (p-) levels of IL-16 in predefined patient groups using ELISA: LN (n=84), active non-renal SLE (n=63), inactive non-renal SLE (n=73) and matched population controls (n=48). The LN group included patients with recent biopsy-confirmed proliferative (PLN, n=47), mesangioproliferative (MES, n=11) and membranous (MLN, n=26) LN. Renal expression of IL-16 was investigated by immunohistochemistry. Associations between IL-16 measurements and clinical parameters and the diagnostic value for LN were explored. Results: p-IL-16 was detected in all investigated cases and high p-IL-16 levels were observed in patients with active SLE. u-IL-16 was detected (dt-u-IL-16) in 47.6% of patients with LN, while only up to 17.8% had dt-u-IL-16 in other groups. In the LN group, 68% of patients with PLN had dt-u-IL-16, while the proportions in the MLN and MES groups were lower (11.5% and 45.5%, respectively). The highest u-IL-16 levels were detected in the PLN group. In the regression model, u-IL-16 levels differentiated PLN from other LN patient subgroups (area under the curve 0.775-0.896, p<0.0001). dt-u-IL-16 had superior specificity but slightly lower sensitivity than elevated anti-double-stranded DNA and low complement C3 or C4 in diagnosing PLN. A high proportion of LN kidney infiltrating cells expressed IL-16. Conclusions: We demonstrate that detectable u-IL-16 can differentiate patients with PLN from those with less severe LN subtypes and active non-renal SLE. Our findings suggest that u-IL-16 could be used as a screening tool at suspicion of severe LN. Furthermore, the high IL-16 levels in plasma, urine and kidney tissue imply that IL-16 could be explored as a therapeutic target in SLE.
MeSH term(s)	Biomarkers ; Humans ; Interleukin-16/urine ; Interleukins/urine ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/diagnosis ; Lupus Nephritis
Chemical Substances	Biomarkers ; Il16 protein, human ; Interleukin-16 ; Interleukins
Language	English
Publishing date	2022-09-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2779620-6
ISSN	2053-8790
ISSN	2053-8790
DOI	10.1136/lupus-2022-000744
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Article ; Online: Regional european genetic ancestry predicts type I interferon level and risk of severe viral infection.

Nln, Ilona / Shum, Justine / Ghodke-Puranik, Yogita / Tipon, Regine / Triese, Danielle / Amin, Shreyasee / Makol, Ashima / Osborn, Thomas / Chowdhary, Vaidehi / Thanarajasingam, Uma / Wampler Muskardin, Theresa L / Oke, Vilija / Gunnarsson, Iva / Zickert, Agneta / Zervou, Maria I / Boumpas, Dimitrios T / Svenungsson, Elisabet / Goulielmos, George N / Niewold, Timothy B

QJM : monthly journal of the Association of Physicians

2024

Abstract: Background: Viral infection outcomes vary widely between individuals, ranging from mild symptoms to severe organ failure and death, and it is clear that host genetic factors play a role in this variability. Type I interferon (IFN) is a critical anti- ... ...

Abstract	Background: Viral infection outcomes vary widely between individuals, ranging from mild symptoms to severe organ failure and death, and it is clear that host genetic factors play a role in this variability. Type I interferon (IFN) is a critical anti-viral cytokine, and we have previously noted differences in type I IFN levels between world populations. Methods: In this study, we investigate the interrelationship between regional European genetic ancestry, type I IFN levels, and severe viral infection outcomes. Results: In cohorts of European ancestry lupus patients living in Europe, we noted higher IFN in the Northwestern populations as compared to Southeastern populations. In an independent cohort of European ancestry lupus patients from the United States with varying proportional regional European genetic admixture, we observed the same Northwest vs. Southeast European ancestry IFN gradient. We developed a model to predict type I IFN level based on regional European ancestry (AUC = 0.73, p = 6.1e-6). Examining large databases containing serious viral outcomes data, we found that lower predicted IFN in the corresponding European country was significantly correlated with increased viral infection fatality rate, including COVID-19, viral hepatitis, and HIV [Correlation coefficients: -0.79 (p = 4e-2), -0.94 (p = 6e-3), and -0.96 (p = 8e-2) respectively]. Conclusions: This association between predicted type I IFN level and viral outcome severity suggests a potential causal relationship, as greater intrinsic type I IFN is beneficial in host defense against viruses. Genetic testing could provide insight into individual and population level risk of fatality due to viruses prior to infection, across a wide range of viral pathogens.
Language	English
Publishing date	2024-03-26
Publishing country	England
Document type	Journal Article
ZDB-ID	1199985-8
ISSN	1460-2393 ; 0033-5622 ; 1460-2725
ISSN (online)	1460-2393
ISSN	0033-5622 ; 1460-2725
DOI	10.1093/qjmed/hcae052
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Article ; Online: Erratum to: Interferon activation status underlies higher antibody response to viral antigens in patients with systemic lupus erythematosus receiving no or light treatment.

Björk, Albin / Da Silva Rodrigues, Rui / Richardsdotter Andersson, Elina / Ramírez Sepúlveda, Jorge I / Mofors, Johannes / Kvarnström, Marika / Oke, Vilija / Svenungsson, Elisabet / Gunnarsson, Iva / Wahren-Herlenius, Marie

Rheumatology (Oxford, England)

2020 Volume 60, Issue 3, Page(s) 1575

Language	English
Publishing date	2020-12-29
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	1464822-2
ISSN	1462-0332 ; 1462-0324
ISSN (online)	1462-0332
ISSN	1462-0324
DOI	10.1093/rheumatology/keaa867
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Article ; Online: The immunobiology of Ro52 (TRIM21) in autoimmunity: a critical review.

Oke, Vilija / Wahren-Herlenius, Marie

Journal of autoimmunity

2012 Volume 39, Issue 1-2, Page(s) 77–82

Abstract: Ro52 is a common target of circulating autoantibodies in autoimmune disease. Data indicate that anti-Ro52 antibodies are associated with distinct clinical manifestations. It is therefore of major interest to understand how it becomes an antigenic target ... ...

Abstract	Ro52 is a common target of circulating autoantibodies in autoimmune disease. Data indicate that anti-Ro52 antibodies are associated with distinct clinical manifestations. It is therefore of major interest to understand how it becomes an antigenic target and what cells express this protein under what conditions and what cellular function it has. Ro52 contains a RING and a B-box motif, followed by a coiled-coil domain and a B30.2 (or PRYSPRY) region in the C-terminal end. This molecular structure places Ro52 within the family of tripartite motif proteins (TRIM), and it is also denoted TRIM21. Like several other TRIM proteins, Ro52 has E3 ligase activity and functions in the process of ubiquitination. Ro52 is expressed in the immune system as a predominantly cytoplasmic protein that can be upregulated and translocate to the nucleus in a proinflammatory environment. Reported substrates for Ro52-mediated ubiquitination include IRF3, IRF5, IRF7 and IRF8, and via these transcription factors Ro52 regulates type 1 interferon and cytokine production. Ro52 is upregulated at the site of autoimmune inflammation, such as cutaneous lupus lesions. This implies that Ro52 may have an important role in the pathogenesis of autoimmunity, and this paper will review the available data on the role of Ro52 in immune responses and autoimmune pathogenesis.
MeSH term(s)	Animals ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmunity ; Humans ; Interferon Regulatory Factor-3/metabolism ; Interferon Regulatory Factor-7/metabolism ; Interferon Regulatory Factors/metabolism ; Ribonucleoproteins/immunology ; Ribonucleoproteins/metabolism ; Ubiquitination
Chemical Substances	IRF3 protein, human ; IRF5 protein, human ; IRF7 protein, human ; Interferon Regulatory Factor-3 ; Interferon Regulatory Factor-7 ; Interferon Regulatory Factors ; Ribonucleoproteins ; SS-A antigen ; interferon regulatory factor-8
Language	English
Publishing date	2012-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2012.01.014
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Article ; Online: Proteome study of cutaneous lupus erythematosus (CLE) and dermatomyositis skin lesions reveals IL-16 is differentially upregulated in CLE.

Niewold, Timothy B / Meves, Alexander / Lehman, Julia S / Popovic-Silwerfeldt, Karin / Häyry, Aliisa / Söderlund-Matell, Therese / Charlesworth, Cristine M / Madden, Benjamin / Lundberg, Ingrid E / Wahren-Herlenius, Marie / Svenungsson, Elisabet / Oke, Vilija

Arthritis research & therapy

2021 Volume 23, Issue 1, Page(s) 132

Abstract: Background: The objective of the study was to explore the disease pathways activated in the inflammatory foci of skin lesions in cutaneous lupus erythematosus (CLE) and dermatomyositis (DM).: Methods: Skin biopsies acquired from active CLE and DM ... ...

Abstract	Background: The objective of the study was to explore the disease pathways activated in the inflammatory foci of skin lesions in cutaneous lupus erythematosus (CLE) and dermatomyositis (DM). Methods: Skin biopsies acquired from active CLE and DM lesions, patient (PC), and also healthy controls (HC) were investigated. Biopsy sections were examined by a pathologist, inflammatory foci were laser micro-dissected and captured, and proteins within captured tissue were detected in an unbiased manner by mass spectrometry. Protein pathway analysis was performed by the string-db.org platform. Findings of interest were confirmed by immunohistochemistry (IHC). Results: Proteome investigation identified abundant expression of interferon-regulated proteins (IRP) as a common feature of CLE and DM. Interleukin (IL)-16 was the only abundant cytokine differentially expressed in CLE compared to DM. Caspase-3, an enzyme that cleaves IL-16 into its active form, was detected in low levels. Significantly higher proportion of IL-16- and caspase-3-positive cells was identified in CLE lesions in comparison with DM, PC, and HC. Proteomic results indicate more abundant complement deposition in CLE skin lesions. Conclusions: Using unbiased mass spectrometry investigation of CLE and DM inflammatory infiltrates, we confirmed that high IRP expression is a common feature of both CLE and DM, while IL-16 is the only differentially expressed cytokine in CLE. IHC confirmed high expression of IL-16 and caspase-3 in CLE. Our novel molecular findings indicate that IL-16 detection could be useful in differential diagnostics between the two conditions that can display similar histopathological appearance. IL-16 could be of interest as a future therapeutic target for CLE.
MeSH term(s)	Dermatomyositis/genetics ; Humans ; Interleukin-16/genetics ; Lupus Erythematosus, Cutaneous/genetics ; Proteome ; Proteomics ; Skin
Chemical Substances	Il16 protein, human ; Interleukin-16 ; Proteome
Language	English
Publishing date	2021-04-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-021-02511-0
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Article: Sjögren Syndrome in Systemic Lupus Erythematosus: A Subset Characterized by a Systemic Inflammatory State.

Ruacho, Guillermo / Kvarnström, Marika / Zickert, Agneta / Oke, Vilija / Rönnelid, Johan / Eketjäll, Susanna / Elvin, Kerstin / Gunnarsson, Iva / Svenungsson, Elisabet

The Journal of rheumatology

2019 Volume 47, Issue 6, Page(s) 865–875

Abstract: Objective: An often-neglected subset of patients with systemic lupus erythematosus (SLE) is those with secondary Sjögren syndrome (SLE-sSS). Further, primary SS overlaps and can be difficult to delineate from SLE. To shed light on the SLE-sSS subset, we ...

Abstract	Objective: An often-neglected subset of patients with systemic lupus erythematosus (SLE) is those with secondary Sjögren syndrome (SLE-sSS). Further, primary SS overlaps and can be difficult to delineate from SLE. To shed light on the SLE-sSS subset, we investigated a large and well-characterized SLE cohort, comparing patients with SLE-sSS and SLE patients without SS (SLE-nonsSS) and controls. Methods: We included 504 consecutive patients with SLE, fulfilling the 1982 revised American College of Rheumatology criteria, and 319 controls from the general population, matched for age and sex to the first 319 patients. SLE-sSS was defined according to the American-European Consensus Criteria (AECC). A thorough clinical examination, including subjective and objective quantifications of sicca symptoms, was performed in all participants. Autoantibodies and 20 selected cytokines were measured by luminex and multiplex analysis, respectively. Results: SLE-sSS, as defined by AECC, occurred in 23% of the patients with SLE. In comparison to SLE-nonsSS, the SLE-sSS group was older and more frequently female. Leukopenia and peripheral neuropathy were more frequent and nephritis less frequent. Circulating levels of 6/20 investigated proinflammatory cytokines [tumor necrosis factor-α, interleukin (IL) 6, monocyte chemoattractant protein 4, macrophage inflammatory protein 1β, IL-12/IL-23p40, and interferon γ-induced protein 10], total IgG, anti-SSA/Ro52, anti-SSA/Ro60, anti-SSB/La antibodies, and rheumatoid factor (IgM and IgA) were higher in the SLE-sSS group (p < 0.05 for all comparisons). Conclusion: The frequency of SLE-sSS increased with age and affected roughly one-quarter of all patients with SLE. Despite less internal organ involvement, a systemic inflammatory state with high levels of proinflammatory cytokines is present in the SLE-sSS subgroup. This is a novel observation that may affect future understanding and treatment of the SLE-sSS subset.
MeSH term(s)	Antibodies, Antinuclear ; Autoantibodies ; Cohort Studies ; Female ; Humans ; Lupus Erythematosus, Systemic/complications ; Sjogren's Syndrome/complications
Chemical Substances	Antibodies, Antinuclear ; Autoantibodies
Language	English
Publishing date	2019-09-15
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	194928-7
ISSN	1499-2752 ; 0315-162X
ISSN (online)	1499-2752
ISSN	0315-162X
DOI	10.3899/jrheum.190250
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Article ; Online: High levels of circulating interferons type I, type II and type III associate with distinct clinical features of active systemic lupus erythematosus.

Oke, Vilija / Gunnarsson, Iva / Dorschner, Jessica / Eketjäll, Susanna / Zickert, Agneta / Niewold, Timothy B / Svenungsson, Elisabet

Arthritis research & therapy

2019 Volume 21, Issue 1, Page(s) 107

Abstract: Background and aim: Interferons (IFNs) are considered to be key molecules in the pathogenesis of systemic lupus erythematosus (SLE). We measured levels of type I, II and III IFNs in a large cohort of patients with systemic lupus erythematosus (SLE) and ... ...

Abstract	Background and aim: Interferons (IFNs) are considered to be key molecules in the pathogenesis of systemic lupus erythematosus (SLE). We measured levels of type I, II and III IFNs in a large cohort of patients with systemic lupus erythematosus (SLE) and controls and explored associations among high levels of different IFN types and distinct SLE features. Methods: Four hundred ninety-seven well-characterized SLE patients and 322 population controls were included. Disease activity was assessed by SLE Disease Activity Index (SLEDAI) and Systemic Lupus Activity Measure (SLAM). Functional type I IFN activity was estimated by a WISH reporter cell assay. Levels of IFN-γ were estimated by MSD 30-plex assay. IFN-α and IFN-λ1 were measured by ELISA. Values above the third quartile of patients' measurements were defined as high. Associations among high IFN results and SLE features were investigated by nominal regression analysis. Results: All IFN measurements were higher in SLE patients than in controls. High type I IFN activity correlated with levels of IFN-γ and IFN-α and associated with active SLE in most domains: weight loss, fatigue, fever, rash, lymphadenopathy, arthritis, nephritis and haematological manifestations. Specific SLE subsets were linked to the upregulation of different subtypes of circulating IFNs: high IFN-γ to arthritis, nephritis and anti-Ro60 antibodies and high IFN-α to mucocutaneous engagement and anti-Ro52 and anti-La antibodies. Isolated high IFN-λ1 was coupled to anti-nucleosome antibodies and less severe SLE. Conclusions: High functional type I IFN activity captures active SLE in most domains, but more distinct patterns of organ involvement are associated with profiles of circulating IFNs. High IFN-γ as well as high functional type I IFN activity is a characteristic of severe SLE with nephritis and arthritis, while elevated levels of IFN-α associate with active mucocutaneous inflammation and a more benign cardiovascular profile. IFN-λ1 in isolation is associated with milder disease. Our findings suggest that IFNs contribute to the heterogeneity of clinical manifestations in SLE, and measuring circulating IFNs could assist in designing clinical trials with therapies targeting IFN pathways.
MeSH term(s)	Adult ; Biomarkers/blood ; Cohort Studies ; Cross-Sectional Studies ; Female ; Humans ; Interferon Type I/blood ; Interferon-gamma/blood ; Interferons/blood ; Lupus Erythematosus, Systemic/blood ; Lupus Erythematosus, Systemic/diagnosis ; Male ; Middle Aged
Chemical Substances	Biomarkers ; Interferon Type I ; interferon type III ; Interferon-gamma (82115-62-6) ; Interferons (9008-11-1)
Language	English
Publishing date	2019-04-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-019-1878-y
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito