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Type I interferon signature in Sjögren's syndrome: pathophysiological and clinical implications.

08:00 EDT 11th July 2019 | BioPortfolio

Summary of "Type I interferon signature in Sjögren's syndrome: pathophysiological and clinical implications."

Type I interferons (IFN) have long been recognised as mediators of innate immune defense mechanisms against viral threats. Robust evidence over the last 15 years revealed their significant role in the pathogenesis of systemic autoimmune diseases, including systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). Despite the progress, methods of detection, initial triggers, biological functions and clinical associations in the setting of autoimmunity remain to be fully clarified. As therapeutic options for SS are currently limited, neutralising specific targets of the type I IFN pathway seems a promising option. In this review we summarise the current evidence regarding the role of type I IFN in SS.

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Name: Clinical and experimental rheumatology
ISSN: 0392-856X
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Medical and Biotech [MESH] Definitions

Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA).

An interferon regulatory factor that binds upstream TRANSCRIPTIONAL REGULATORY ELEMENTS in the GENES for INTERFERON-ALPHA and INTERFERON-BETA. It functions as a transcriptional activator for the INTERFERON TYPE I genes.

A type II interferon produced by recombinant DNA technology. It is similar to the interferon secreted by lymphocytes and has antiviral and antineoplastic activity.

A type I interferon with antiviral and antineoplastic activity produced by recombinant DNA technology. It can be a mixture of alpha and beta interferons.

The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.

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