Autoimmune (immunoinflammatory) rheumatic diseases are defined as clinical syndromes whose development is associated with the abnormal activation of T cells, B cells, and many other cells of the immune system, which gives rise to the progressive inflammation and destruction of the viscera. In spite of the high efficiency of combined therapy with biologic agents and standard disease-modifying antirheumatic drugs, primarily methotrexate, less than half of patients with rheumatoid arthritis (RA) could achieve a significant clinical effect and, very rarely, sustained remission. The combined influence of genetic and environmental factors may lead to loss of immunological tolerance, the basis for which is an imbalance between the effector and regulatory components of the immune system. To restore tolerance without chronic nonspecific immunosuppression observed in the use of majority of current anti-inflammatory drugs (including GEBAs) is regarded as the most important task of pharmacotherapy for RA. The aim of the review is to discuss firstly the role of the so-called T regulatory (Treg) cells as one of the critical components for the maintenance of tolerance and secondly promises for the pharmacotherapy of RA associated with the correction of the functional activity of Treg cells.

Matrix metalloproteinases (MMPs) are a group of over 20 proteolytic enzymes responsible for cleavage of protein components of the extracellular matrix. Three types of MMPs play an important role in the development of joint damage in patients with rheumatoid arthritis (RA): collagenases (MMP1, 8 and 13), stromelysins (MMP3), and gelatinases (MMP9). MMP3 is considered to be one of the key mediators of joint damage. Increased serum level of MMP is not specific for RA and may be registered in other rheumatic diseases (osteoarthritis, psoriatic arthritis, gout, ankylosing spondylitis, systemic lupus erythematosus); however, monitoring of the level of MMP is of particular clinical importance in patients with RA. MMP3 serum level may be a useful marker of disease activity. Several studies have shown a correlation of MMP3 concentration with clinical and laboratorial parameters of inflammatory activity (ESR and C-reactive protein – CRP) in RA patients. The elevated level of MMP3 is associated with radiological changes in joints and can also be a predictor of severe destructive lesions in RA patients. Evaluation of the MMP3 level can also be useful for monitoring the therapy effectiveness using both standard disease-modifying antirheumatic drugs (DMARDs) and genetically engineered biological drugs (GEBD). Thus, evaluation of MMP3 concentration is useful for assessing disease activity and efficacy of treatment with DMARDs and GEBD, as well as for predicting the severity of destructive changes in joints.