Rheumatoid arthritis (RA) is a systemic, inflammatory, autoimmune disorder with 
progressive articular damage that may result in lifelong disability. Although 
major strides in understanding the disease have been made, the pathogenesis of 
RA has not yet been fully elucidated. Early treatment can prevent severe 
disability and lead to remarkable patient benefits, although a lack of 
therapeutic efficiency in a considerable number of patients remains problematic. 
MicroRNAs (miRNAs) are small, non-coding RNAs that, depending upon base pairing 
to messenger RNA (mRNA), mediate mRNA cleavage, translational repression or mRNA 
destabilization. As fine tuning regulators of gene expression, miRNAs are 
involved in crucial cellular processes and their dysregulation has been 
described in many cell types in different diseases. In body fluids, miRNAs are 
present in microvesicles or incorporated into complexes with Argonaute 2 (Ago2) 
or high-density lipoproteins and show high stability. Therefore, they are of 
interest as potential biomarkers of disease in daily diagnostic applications. 
Targeting miRNAs by gain or loss of function approaches have brought therapeutic 
effects in various animal models. Over the past several years it has become 
clear that alterations exist in the expression of miRNAs in patients with RA. 
Increasing numbers of studies have shown that dysregulation of miRNAs in 
peripheral blood mononuclear cells or isolated T lymphocytes, in synovial tissue 
and synovial fibroblasts that are considered key effector cells in joint 
destruction, contributes to inflammation, degradation of extracellular matrix 
and invasive behaviour of resident cells. Thereby, miRNAs maintain the 
pathophysiological process typical of RA. The aim of the current review is to 
discuss the available evidence linking the expression of miRNAs to inflammatory 
and immune response in RA and their potential as biomarkers and the novel 
targets for treatment in patients with RA.