AI Article Synopsis
- Abnormal interferon type I production is linked to autoimmune diseases like systemic lupus erythematosus (SLE), marked by high levels of type I interferon-related genes.
- Interferon regulatory factors (IRFs), crucial for immune responses and cell development, have been studied in animal models but have limited human data.
- The review emphasizes IRF-5 and IRF-7's roles in autoimmune disease susceptibility, particularly their strong association with SLE pathology.
Article Abstract
Abnormal production of interferon type I has been widely related to multiple autoimmune diseases, particularly systemic lupus erythematosus (SLE). It has been considered the molecular signature characterized by the overexpression of type I Interferon related genes in SLE patients. Among these, are the interferon regulatory factors (IRF). These transcription factors have been involved in the innate immune response, mainly the one related to the defense against viral infections; the development of immune cells and carcinogenesis. The role of IRF in autoimmune pathology has been addressed in diverse murine models. However, evidence in humans is quite scant. This review will focus on the evidence that supports the role of IRF in the development or susceptibility to autoimmune diseases. Specific emphasis will be made over the role of IRF-5 and IRF-7, since evidence of its association to the development of pathology, particularly systemic lupus erythematosus is the strongest.
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| http://dx.doi.org/10.1016/j.autrev.2011.08.006 | DOI Listing |
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