Systemic lupus erythematosus (SLE) is a chronic, heterogenous, systemic autoimmune disease characterized by autoantibody production, complement activation, and immune complex deposition. It predominantly affects young and middle-aged, child-bearing women. While upgrades in treatment and diagnosis have been made in SLE resulting in altered prognosis, morbidity and mortality remain better in the overall population.

The disease pathology involves innate and adaptive immune dysregulation.In 2011, a working party organized by the Lupus Foundation of America defined a flare in a lupus patient as a measurable increase in disease activity in one or more organ systems involving new or worse clinical signs and symptoms and/or laboratory measurements.[5] In spite of many attempts performed to comprehend the pathogenesis of SLE, there is still a deficiency of adequate knowledge about the precise mechanisms underlying the disease to develop effective therapies for SLE patients. micro-RNAs (miRNAs) have been implicated in the development of SLE by the recent studies.

Genetic and environmental factor plays an important role in leading SLE. miRNA dysfunction leads to autoimmunity. miRNA-mediated B cell and T cells lead to SLE pathogenies. Different miRNAs miR-126, miR-21, miR-146a, miR-155, and miR-1246 gene expression by epigenetic modifications, differentiation of cell subsets, B cell hyperactivity and autoantibody production is seen.  miR-146a gene polymorphism has been seen as SLE genetic basis which varies across populations.Distinct miRNAs are differentially expressed in both SLE mice models and human patients. miRNAs are important targeting molecules modulating susceptibility to SLE.

Micro-RNAs are small non-coding RNAs that regulate gene expression at both transcriptional and translation levels. They play a crucial role in the development of the immune system, and as the regulator of both the innate and adaptive immune systems. Altered expressions of miRNAs are seen in autoimmune diseases such as SLE. Considering this, miRNAs have become an area of interest owing to their contributory role in disease pathogenesis. In SLE, there is an activation of both the innate and adaptive immune systems, and specific miRNAs are linked to some key processes involving both.

Some of these processes include: interference in the Type 1 Interferon (IFN)-signalling

pathway (miR-146a, miR-155) DNA hypo-methylation in T cells (miR-21, miR-126, miR-148a) (aberration in inflammatory chemokine pathways (miR-125a) neutrophil development and function (miR125a, miR223, miR451a) B-cell hyperstimulation and T-cell over-activation (miR-142-3p/5p) (16 ); induction of regulatory T cells (miR-16) and regulation of myeloid cell development ( miR-223) 

With the new insights about miRNA’s involvement in SLE, studies have determined the differential expression in SLE. Most of the profiling studies have been done on Caucasian and Asian populations. However, there are no studies that have profiled miRNA expression patterns in Indian SLE patients during flare and remission. In addition, specific miRNA expression signatures in SLE flare with response to different drugs have not been studied.

So, we hypothesize that micro RNAs are differentially expressed in SLE patients compared to healthy individuals in remission and exacerbation. The differences in the expression of miRNAs may contribute to the pathophysiology of SLE. The purpose of our study is to determine the overall expression of plasma miRNAs in a group of the Indian population.