Immune Interferon in the Circulation of Patients with Autoimmune Disease

Hooks, John J.; Moutsopoulos, Haralampos Μ.; Geis, Shirley A.; Stahl, Neil; Decker, John L.; Notkins, Abner Louis

doi:10.1056/nejm197907053010102

Cited by 815 publications

(466 citation statements)

References 18 publications

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“…Although modulation of EPC numbers has been identified in the course of cardiovascular disease or vascular trauma (which appears to be predictive of clinical coronary events in the general population), there is still much controversy regarding their true identity and role. In SLE, while most of the studies demonstrated low percentages of circulating EPC (Lee et al, 2007;Moonen et al, 2007;Westerweel et al, 2007;Robak et al, 2009), results are inconsistent, most likely due to different protocols adopted for identifying EPC (Hooks et al, 1979). Nevertheless, whether the number of circulating EPC can predict cardiovascular events in patients with SLE remains to be answered by prospective studies.…”

Section: Epc In Slementioning

confidence: 99%

Endothelial progenitor cells: Are they displaying a function in autoimmune disorders?

Ferrante

Guggino

Liberto

et al. 2016

Mechanisms of Ageing and Development

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a b s t r a c tEndothelial Progenitor Cells (EPCs) are bone marrow derived cells able to differentiate in mature endothelial cells (EC) contributing to the generation of new vessels, connecting to fibronectin, and forming colonies and/or colony forming units.Since circulating EPCs can be actively considered part of endothelial damage in several cardiovascular diseases and autoimmune disorders the possibility to have a measure for endothelium damage should be considered of interest to predict the patient out-come. At the same time the EPCs proliferative and regenerative role could be considered for therapeutic applications.

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Section: Epc In Slementioning

confidence: 99%

Endothelial progenitor cells: Are they displaying a function in autoimmune disorders?

Ferrante

Guggino

Liberto

et al. 2016

Mechanisms of Ageing and Development

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show abstract

“…It has been known for more than 25 years that patients with SLE have elevated serum IFN␣ levels (36), and that these levels correlate to both disease activity and severity (36)(37)(38). There is also a correlation between serum IFN␣ levels and several markers of immune activation typical for SLE, e.g., anti-dsDNA titers, IL-10 levels, and degree of complement activation.…”

Section: Introductionmentioning

confidence: 99%

The type I interferon system in systemic lupus erythematosus

Rönnblom

Eloranta

Alm

2006

Arthritis & Rheumatism

301

246

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“…A series of studies using microarray gene expression analysis in patient peripheral blood cells demonstrated an 'IFN signature' in SLE, which correlated with renal and hematological involvement of phenotypes. [1][2][3][4][5][6] Supporting evidence has also come from studies on murine lupus. The (New Zealand Black (NZB) Â New Zealand White (NZW))F1 hybrid female mice (NZB/W) develop a disease closely resembling human SLE, characterized by the production of antinuclear antibodies, severe glomerulonephritis and early mortality.…”

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confidence: 98%

Genomic view of IFN-α response in pre-autoimmune NZB/W and MRL/lpr mice

Shen

et al. 2007

Genes Immun

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Interferon (IFN)-a is involved in the pathogenesis of systemic lupus erythematosus. Studies in murine lupus models have revealed that type I IFN exerts either a protective effect in MRL/lpr, or can detrimentally impact disease progression, as in NZB/ W mice. To understand this paradox, we examined the kinetic global gene expression in pre-autoimmune NZB/W-, MRL/lprand normal BALB/c-derived splenic mononuclear cells following ex vivo IFN-a treatment. Analysis of IFN-a-induced gene expression patterns revealed genes associated with antiproliferative activity of IFN-a including CDKN1A, GADD45B, pituitary tumor-transforming 1, SCOTIN, ataxia telangiectasia-mutated homolog and calcyclin-binding protein were upregulated in MRL/ lpr and/or BALB/c mice. Of IFN-a-induced genes differentially expressed in NZB/W vs BALB/c and MRL/lpr mice at 3 h time point, enhanced expression of CCND1, cyclin D2, matrix metalloproteinase 13 and a panel of cytokines and chemokines and impaired expression of negative inflammatory regulators CD69 and an Src family kinase hemopoietic cell kinase were notable. Interestingly, the splenic mononuclear cells from the NZB/W not MRL/lpr lupus-prone mice at the pre-autoimmune stage before ex vivo IFN-a treatment, have increased expression of many known IFN-regulated genes. These results provide a unique genomic view of ex vivo IFN-a response in two lupus-prone models, and help to have an insight into the role of IFN-a in lupus pathogenesis Genes and Immunity (2007) IntroductionSystemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease characterized by a break of immune tolerance to self antigens, resulting in inflammation and damage to a range of organ systems. The exact pathoetiology of SLE remains elusive. Elevated serum levels of IFN-a have long been observed and correlated with disease activity. A series of studies using microarray gene expression analysis in patient peripheral blood cells demonstrated an 'IFN signature' in SLE, which correlated with renal and hematological involvement of phenotypes. [1][2][3][4][5][6] Supporting evidence has also come from studies on murine lupus. The (New Zealand Black (NZB) Â New Zealand White (NZW))F1 hybrid female mice (NZB/W) develop a disease closely resembling human SLE, characterized by the production of antinuclear antibodies, severe glomerulonephritis and early mortality. In the NZB parental strain, which also develops a lupus-like syndrome, homozygous IFN-a/b R-deleted NZB mice had significantly reduced antierythrocyte autoantibodies, erythroblastosis, hemolytic anemia, anti-DNA autoantibodies, kidney disease and mortality. 7 In contrast to normal BALB/c mice, continuous in vivo treatment of IFN-a in pre-autoimmune NZB/W mice from 8 weeks of age precipitates the autoimmune process and kidney damage, leading to premature death from severe immune complex glomerulonephritis. This result provides a direct evidence that IFN-a is implicated in the pathogenesis of SLE. 8 Thus, the type I IFNs have emerged as a dominant target in the path...

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Immune Interferon in the Circulation of Patients with Autoimmune Disease

Cited by 815 publications

References 18 publications

Endothelial progenitor cells: Are they displaying a function in autoimmune disorders?

Endothelial progenitor cells: Are they displaying a function in autoimmune disorders?

The type I interferon system in systemic lupus erythematosus

Genomic view of IFN-α response in pre-autoimmune NZB/W and MRL/lpr mice

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