Aim: The aim of this dissertation was to explore the influence of immune system on pathogenesis of spondyloarthritis (SpA), with special consideration to eripheral blood mononuclear cells (PBMC) and the role of vitamin D. Material and methods: Research was performed both on the basis of Polish Spondyloarthritis Initiative (PolSPI) and as a part of project supported by National Centre of Science which is concerned to the role of peripheral blood mononuclear cells in bone remodeling in spondyloarthritis. Results: We found that patients with peripheral SpA have decreased number of circulating nonclassical monocytes in comparison with controls and that there is a significant negative correlation between the concentration of nonclassical monocytes and DAS28 and the number of swollen joints. In a group of axial SpA patients, sera levels of soluble RANKL were significantly lower and M-CSF, IL-6, OSM, IL-17A and TNFα significantly higher in comparison to controls. Monocytes isolated from healthy donors, cultured in the presence of sera from axSpA patients had significantly higher differentiation to osteoclast compared to monocytes cultured in sera of healthy donors.We didn’t observed correlation between concentration of vitamin D and activity of SpA when assessing disease activity scores (BASDAI, ASDAS), inflammatory markers (CRP, ESR) and clinical manifestation (peripheral arthritis, enthesitis, dactylitis). These results didn’t change after adjustment for seasonal variation and supplementation of vitamin D. Conclusions: Our research indicates significant role of non-classical monocytes in the pathogenesis of SpA, especially in peripheral arthritis. Monocytes differentiation into osteoclasts is mediated not only by RANKL stimulation (canonical pathway) but also by other soluble factors such as IL-6, OSM, IL-17A and TNFα (non-canonical pathway) which sensitize osteoclasts for RANKL stimulation. The influence of vitamin D in recommended concentration on immunological processes in SpA seems to be of little importance.