Rheumatoid arthritis (RA) is a chronic autoimmune systemic disease characterized predominantly by synovial inflammation, leading to joint destruction. RA affects up to 1% of the population in the world and is associated with reduced life expectancy (1). The synovium in RA transforms into inflammatory tissue, called pannus, which produces several proinflammatory mediators and invades cartilage and bone. Pannus formation is caused by the proliferation of fibroblast-like synovial cells and synoviocytes, angiogenesis, infiltration of macrophages and lymphocytes and migration of polymorphonuclear cells to the synovial tissue (2). Interleukin 1 (IL-1), tumor necrosis factor (TNF-α) and interleukin 6 (IL-6) play a primary role in mediating this process. One of the important mechanisms of RA pathophysiology is the imbalance between Th1 and Th2 response with Th1 predominance (interleukin 2 and interferon γ excretion). The other significant inflammatory pathway is associated with Th17 cells and characterized by production of IL-17A, IL-17F, TNF and IL-6 (3). The risk factors for RA development involve the combination of genetic and environmental components. The most important genetic factor is associated with the major histocompatibility complex antigen HLA-DRB1 and shared epitope, which is closely related to serum presence of rheumatoid factor (RF) or anti-citrullinated peptide antibodies (a-CCP) (4, 5). Of the environmental stimuli that contribute, the best defined is smoking, which can interact with genes to increase disease susceptibility (4). One of the other possible environmental factors is vitamin D. Despite being a crucial element of calcium homeostasis and bone mineralization, vitamin D also plays an important role in immune system. The expression of vitamin D receptor (VDR) was discovered on antigen-presenting cells, dendritic cells and lymphocytes. VDR has been demonstrated in the rheumatoid synovium and macrophages derived from RA patients are capable to vitamin D synthesis (6). Active metabolite of vitamin D, calcitriol (1,25-dihydroxyvitamin D) can inhibit the macrophage synthesis of interleukines 1, 6, 12 and TNF-α, suppress the interleukin 2 secretion by Th1 lymphocytes and decrease antigen-presenting activity of macrophages – therefore restoring balance between Th1, Th17 and Th2 cells (7). Furthermore, calcitriol inhibits plasma-cell differentiation and B-cell proliferation (8). Vitamin D deficiency is more common in autoimmunological diseases than in general population (9). These observations were the reason for numerous studies on the role of vitamin D deficiency in the occurrence, activity and severity of RA.