Analysis of interferon type I signature for differential diagnosis of diseases of the immune system ( review of literature)

2021 ◽  
Vol 66 (5) ◽  
pp. 279-284
Author(s):  
E. N. Suspitsin ◽  
R. K. Raupov ◽  
E. M. Kuchinskaya ◽  
M. M. Kostik
Keyword(s):  
Lupus Erythematosus ◽  
Expression Patterns ◽  
Type I ◽  
Antiviral Defense ◽  
Review Of Literature ◽  
Interferon Signature ◽  
Score Analysis ◽  
System Review ◽  
Diagnosis Of Diseases

Type 1 interferons (IFN1) are both key molecules of antiviral defense and potent inflammatory mediators. In 2003, increased expression of a variety of interferon 1-regulated genes was observed in a blood cells of patients with systemic lupus erythematosus (SLE). This phenomenon was called the type 1 interferon signature (IFN1-signature). Since then, expression patterns indicating the presence of an IFN1-signature were consistently detected in a range of monogenic and complex autoimmune and autoinflammatory conditions. A quantitative indicator reflecting the degree of hyperactivation of the IFN1 pathway is known as interferon score. This review discusses the possible causes of upregulated expression of interferon 1-induced genes, the laboratory approaches to the interferon score analysis, as well as the practical use of this indicator for the diagnosis of various conditions.

scholarly journals An Easy and Reliable Strategy for Making Type I Interferon Signature Analysis Comparable among Research Centers

Diagnostics ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 113 ◽  
Author(s):  
Alessia Pin ◽  
Lorenzo Monasta ◽  
Andrea Taddio ◽  
Elisa Piscianz ◽  
Alberto Tommasini ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Type I Interferon ◽  
Diagnostic Value ◽  
Type I ◽  
Data Normalization ◽  
Signature Analysis ◽  
Interferon Signature ◽  
Interferon Stimulated Genes ◽  
Targeted Treatments ◽  
To Receive

Interferon-stimulated genes (ISGs) are a set of genes whose transcription is induced by interferon (IFN). The measure of the expression of ISGs enables calculating an IFN score, which gives an indirect estimate of the exposition of cells to IFN-mediated inflammation. The measure of the IFN score is proposed for the screening of monogenic interferonopathies, like the Aicardi-Goutières syndrome, or to stratify subjects with systemic lupus erythematosus to receive IFN-targeted treatments. Apart from these scenarios, there is no agreement on the diagnostic value of the score in distinguishing IFN-related disorders from diseases dominated by other types of cytokines. Since the IFN score is currently measured in several research hospitals, merging experiences could help define the potential of scoring IFN inflammation in clinical practice. However, the IFN score calculated at different laboratories may be hardly comparable due to the distinct sets of IFN-stimulated genes assessed and to different controls used for data normalization. We developed a reliable approach to minimize the inter-laboratory variability, thereby providing shared strategies for the IFN signature analysis and allowing different centers to compare data and merge their experiences.

A 17-Year-Old Male with Large Retropharyngeal Neurofibroma as the Only Symptom of Neurofibromatosis Type 1 (NF1): A Case Report and Review of Literature

2019 ◽  
Author(s):  
Heather A. Voss-Hoynes ◽  
Naeem Mahfooz ◽  
Waseem Ostwani
Keyword(s):  
Plexiform Neurofibroma ◽  
Neurofibromatosis Type ◽  
Type I ◽  
Neurofibromatosis Type I ◽  
Review Of Literature ◽  
Unique Case ◽  
Lower Lip ◽  
Head And Neck Imaging ◽  
Extensive Involvement

AbstractRetropharyngeal neurofibromas are rarely described in the literature and are commonly associated with severe airway-related symptoms. We report a unique case of a large retropharyngeal plexiform neurofibroma in an asymptomatic 17-year-old male patient. This patient was asymptomatic and presented for lower lip edema secondary to an insect bite. Head and neck imaging demonstrated an extensive retropharyngeal neurofibroma measuring 5.7 cm × 2.2 cm × 6.8 cm. Because of extensive involvement of cervical vasculature, the lesion was not resected in our institution and his care was referred to a large neurofibromatosis type I center.

scholarly journals New Frontiers: ARID3a in SLE

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1136 ◽  
Author(s):  
Joshua Garton ◽  
M. David Barron ◽  
Michelle L. Ratliff ◽  
Carol F. Webb
Keyword(s):  
Lupus Erythematosus ◽  
Expression Patterns ◽  
Strong Association ◽  
Cell Types ◽  
Peripheral Blood Cell ◽  
Type I ◽  
Interaction Domain ◽  
Autoantibody Production ◽  
Hematopoietic Stem ◽  
Multiple Organs

Systemic lupus erythematosus (SLE) is a devastating and heterogeneous autoimmune disease that affects multiple organs, and for which the underlying causes are unknown. The majority of SLE patients produce autoantibodies, have increased levels of type-I inflammatory cytokines, and can develop glomerulonephritis. Recent studies indicate an unexpected but strong association between increased disease activity in SLE patients and the expression of the DNA-binding protein ARID3a (A + T rich interaction domain protein 3a) in a number of peripheral blood cell types. ARID3a expression was first associated with autoantibody production in B cells; however, more recent findings also indicate associations with expression of the inflammatory cytokine interferon alpha in SLE plasmacytoid dendritic cells and low-density neutrophils. In addition, ARID3a is expressed in hematopoietic stem cells and some adult kidney progenitor cells. SLE cells expressing enhanced ARID3a levels show differential gene expression patterns compared with homologous healthy control cells, identifying new pathways potentially regulated by ARID3a. The associations of ARID3a expression with increased disease severity in SLE, suggest that it, or its downstream targets, may provide new therapeutic targets for SLE.

scholarly journals Functionally impaired plasmacytoid dendritic cells and non-haematopoietic sources of type I interferon characterize human autoimmunity

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Antonios Psarras ◽  
Adewonuola Alase ◽  
Agne Antanaviciute ◽  
Ian M. Carr ◽  
Md Yuzaiful Md Yusof ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell Activation ◽  
Lupus Erythematosus ◽  
Cell Activation ◽  
Type I Interferon ◽  
Connective Tissue Diseases ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Interferon Production ◽  
Interferon Signature

AbstractAutoimmune connective tissue diseases arise in a stepwise fashion from asymptomatic preclinical autoimmunity. Type I interferons have a crucial role in the progression to established autoimmune diseases. The cellular source and regulation in disease initiation of these cytokines is not clear, but plasmacytoid dendritic cells have been thought to contribute to excessive type I interferon production. Here, we show that in preclinical autoimmunity and established systemic lupus erythematosus, plasmacytoid dendritic cells are not effector cells, have lost capacity for Toll-like-receptor-mediated cytokine production and do not induce T cell activation, independent of disease activity and the blood interferon signature. In addition, plasmacytoid dendritic cells have a transcriptional signature indicative of cellular stress and senescence accompanied by increased telomere erosion. In preclinical autoimmunity, we show a marked enrichment of an interferon signature in the skin without infiltrating immune cells, but with interferon-κ production by keratinocytes. In conclusion, non-hematopoietic cellular sources, rather than plasmacytoid dendritic cells, are responsible for interferon production prior to clinical autoimmunity.

scholarly journals Architectural B-cell organization in skeletal muscle identifies subtypes of dermatomyositis

2018 ◽  
Vol 5 (3) ◽  
pp. e451 ◽  
Author(s):  
Josefine Radke ◽  
Randi Koll ◽  
Corinna Preuße ◽  
Debora Pehl ◽  
Kremena Todorova ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
B Cells ◽  
B Cell ◽  
Type I ◽  
Cell Content ◽  
Interferon Signature ◽  
Type 1 Interferon ◽  
Cell Immunity

ObjectiveTo study the B-cell content, organization, and existence of distinct B-cell subpopulations in relation to the expression of type 1 interferon signature related genes in dermatomyositis (DM).MethodsEvaluation of skeletal muscle biopsies from patients with adult DM (aDM) and juvenile DM (jDM) by histology, immunohistochemistry, electron microscopy, and quantitative reverse-transcription PCR.ResultsWe defined 3 aDM subgroups—classic (containing occasional B cells without clusters), B-cell–rich, and follicle-like aDM—further elucidating IM B-lymphocyte maturation and immunity. The quantity of B cells and formation of ectopic lymphoid structures in a subset of patients with aDM were associated with a specific profile of cytokines and chemokines involved in lymphoid neogenesis. Levels of type 1 interferon signature related gene expression paralleled B-cell content and architectural organization and link B-cell immunity to the interferon type I signature.ConclusionThese data corroborate the important role of B cells in DM, highlighting the direct link between humoral mechanisms as key players in B-cell immunity and the role of type I interferon–related immunity.

scholarly journals Acropulpitis in systemic lupus erythematosus is associated with high type 1 interferon signature

2021 ◽  
Author(s):  
Gabrielle Sonigo ◽  
Charles Cassius ◽  
Maxime Battistella ◽  
Hélène Le Buanec ◽  
Martine Bagot ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
High Type ◽  
Interferon Signature ◽  
Type 1 Interferon

Comparative Study of effectiveness of mobilization with movement (MWM) and End range mobilization (ERM) techniques in frozen shoulder

2018 ◽  
Vol 4 (4) ◽  
pp. 519-522
Author(s):  
Jeyakumar S ◽  
Jagatheesan Alagesan ◽  
T.S. Muthukumar
Keyword(s):  
Range Of Motion ◽  
Frozen Shoulder ◽  
Type I ◽  
Mean Values ◽  
Functional Activities ◽  
Group A ◽  
The Mean ◽  
Group B

Background: Frozen shoulder is disorder of the connective tissue that limits the normal Range of motion of the shoulder in diabetes, frozen shoulder is thought to be caused by changes to the collagen in the shoulder joint as a result of long term Hypoglycemia. Mobilization is a therapeutic movement of the joint. The goal is to restore normal joint motion and rhythm. The use of mobilization with movement for peripheral joints was developed by mulligan. This technique combines a sustained application of manual technique “gliding” force to the joint with concurrent physiologic motion of joint, either actively or passively. This study aims to find out the effects of mobilization with movement and end range mobilization in frozen shoulder in Type I diabetics. Materials and Methods: 30 subjects both male and female, suffering with shoulder pain and clinically diagnosed with frozen shoulder was recruited for the study and divided into two groups with 15 patients each based on convenient sampling method. Group A patients received mobilization with movement and Group B patients received end range mobilization for three weeks. The outcome measurements were SPADI, Functional hand to back scale, abduction range of motion using goniometer and VAS. Results: The mean values of all parameters showed significant differences in group A as compared to group B in terms of decreased pain, increased abduction range and other outcome measures. Conclusion: Based on the results it has been concluded that treating the type 1 diabetic patient with frozen shoulder, mobilization with movement exercise shows better results than end range mobilization in reducing pain and increase functional activities and mobility in frozen shoulder.

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