2.3.2. Cytokines as potential biomarkers

As mentioned earlier with SLE pathophysiology, type I interferons and other cytokines exhibit exacerbated activities in SLE and are key players in disease activity [1, 4]. Therefore, such mediators represent potential biomarkers and well-validated therapeutic targets in SLE.

Cytokines with the most characterized roles in SLE pathology are those of type I interferon pathway such as IFN-α and downstream-induced gene products. Aberrantly elevated levels of INF-α have been detected in cerebrospinal fluid of patients with neuropsychiatric disease in systemic lupus erythematosus in comparison to cerebrospinal fluid samples obtained from patients with other autoimmune diseases [81] and were suggested to contribute to disease pathogenicity [82].

Using DNA microarray technology, the expression pattern of IFN-induced genes was found to be highly elevated in peripheral blood mononuclear cells obtained from SLE patients with severe disease state [83]. Positive correlation between IFN-induced genes and severity of SLE clinical manifestations and multiple organ damage was also observed in other studies [84, 85].

Among the most noticeable gene products that are regulated by type I interferons are IP-10 and sialic acid-binding Ig-like lectin 1 which were found to be associated with SLE pathogenicity and were detected in highly elevated levels in many SLE patients [86, 87].

Many other cytokines have been detected in elevated levels in the sera of many SLE patients and can thus represent potential biomarkers including IL-17 [88], IL-6, IL-10, IL-12, IL-15, and IL-21 and others [5, 43].
