expression is largely restricted to the medulla, the development of which seems to parallel the development of Foxp3+ cells. It has been suggested that the two are linked, but no definitive link between the processes has yet been shown. TGF-β is not required for Treg functionality, in the thymus, as thymic Tregs from TGF-β insensitive TGFβRII-DN mice are functional. Thymic recirculation There was observed, that some FOXP3+ Treg cells are recirculating back to thymus, where they have developed. This Treg were mainly present in thymic medula, which is the main site of Treg cells differentiation. The presence of this cells in thymus or addition into fetal thymic tissue culture suppress development of new Treg cells by 34–60%, but Tconv cells are not affected. That means, that recirculating Treg to thymus inhibited just de novo development of Treg cells. Molecular mechanism of this process works due to the ability of Treg to adsorb IL-2 from the microenvironments, thus being able to induce apoptosis of other T cells which need IL-2 as main growth factor. Recirculating T reg cells in thymus express high amount of high affinity IL-2 receptor α chain (CD25) encoded by Il2ra gene which gather IL-2 from thymic medulla, and decrease its concentration. New generated FOXP3+ Treg cells in thymus have not so high amount of Il2ra expression. IL-2 is a cytokine necessary for the development of Treg cells in the thymus. It is important for T cells proliferation and survival, but in the case of its deficiency, IL-15 may be replaced. However, Treg cells' development is dependent on IL-2. In humans, there was found population of CD31 negative Treg cells in thymus. CD31 could be used as a marker of new generated Treg cells as same as other T lymphocytes. Mature and peripheral Treg cells have decreased its expression. So it is possible that this regulatory mechanism of thymic Treg cells development is also functional in humans. There is probably also positive regulation of thymic Treg cells development caused by recirculating Treg cells into thymus. There was found population of CD24 low FOXP3+ in thymus with increased expression of IL-1R2 (Il1r2) compared with peripheral Treg cells. High concentration of IL-1β caused by inflammation decrease de novo development of Treg cells in thymus. The presence of recirculating Treg cells in the thymus with high IL1R2 expression during inflammatory conditions helps to uptake IL-1β and reduce its concentration in the