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They are not expressed in developing T cells but seem to be involved in spleen development.
In the cortex of the thymus, developing T cells, called thymocytes, come to distinguish between the body's own components, referred to as "self," and those substances foreign to the body, called "nonself".
Developing T cells undergo long-range migrations in the thymus that are tightly linked to their developmental program.
Here, we show that in developing T cells, the Bcl11b enhancer repositioned from the lamina to the nuclear interior.
Understanding how these mechanisms contribute to disease susceptibility, particularly in infants with developing T cell repertoires, requires further investigation.
Probably the most obvious candidates for the cells producing IL-2 in the thymus are (developing) T cells.
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Development of both TECs relies on cell-cell interactions between the developing T-lymphocytes and the thymic epithelium.
For instance, E2Ako mice display a high risk of developing T-cell tumors, as do E2AkoId1ko mice.
Moreover, overstimulation of developing T-cells was observed that could potentially induce self-reactive clones escaping the selection process.
Its major function is to eliminate developing T-cells (thymoctyes) whose antigen receptor can bind self antigens and have the potential to cause autoimmune disease [ 1, 2].
This so-called ectopic or promiscuous gene expression significantly broadens the repertoire of self-antigens that can be presented to developing T-cells.
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