The pathogenesis of rheumatoid arthritis (RA) and inflammatory bowel diseases (IBDs) is associated with impaired immunological tolerance. Regulatory T cells (Tregs) play an important role in the regulation of the immune response and can prevent the development of excessive inflammation. Tregs use various immunosuppressive mechanisms to fulfil their function, in particular the adenosine-mediated mechanism associated with the activation of ectonucleotidase ENTPD1 (CD39). Our aim was to study the content of CD39⁺ Treg cells in RA and IBDs. According to our data, high heterogeneity of the CD39 marker is observed in autoimmune diseases. The frequencies of CD4⁺CD25⁺FOXP3⁺ Treg cells themselves were at the control level in RA, while the proportion of CD39⁺ cells was lower. In IBDs, on the contrary, the content of CD4⁺CD25⁺FOXP3⁺ Treg cells was lower, whereas the proportion of CD39+ cells was significantly increased in comparison to both patients with RA and to the healthy control. There was a significant increase in the number of activated T-helpers in both groups of patients compared to the healthy control. The frequency of CD4⁺CD25⁺FOXP3⁺ T cells was higher in RA compared to controls, while in patients with IBDs it was significantly lower. We assume that changes in the subpopulation composition and expression of CD39 are associated with the pathogenesis of inflammatory diseases, since these indicators can be used as markers of the inflammation process.