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Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany; Department of Hematology, Oncology, Klinikum rechts der Isar, Technische Universität München, Ismaninger Straße 15, 81675 Munich, Germany. Electronic address:
Published: November 2014
AI Article Synopsis
Regulatory T (Treg) cells play a key role in maintaining immune balance and preventing harmful immune responses like inflammation and autoimmunity.
Researchers investigated how the self-reactive T cell receptor (TCR) signals influence mature Treg cell functions by genetically altering their TCR in living organisms.
The study found that while TCR signals are crucial for Treg cell maintenance and function, they are not necessary for certain Treg characteristics, like the expression of a defining gene called Foxp3.
Article Abstract
Regulatory T (Treg) cells maintain immune homeostasis and prevent inflammatory and autoimmune responses. During development, thymocytes bearing a moderately self-reactive T cell receptor (TCR) can be selected to become Treg cells. Several observations suggest that also in the periphery mature Treg cells continuously receive self-reactive TCR signals. However, the importance of this inherent autoreactivity for Treg cell biology remains poorly defined. To address this open question, we genetically ablated the TCR of mature Treg cells in vivo. These experiments revealed that TCR-induced Treg lineage-defining Foxp3 expression and gene hypomethylation were uncoupled from TCR input in mature Treg cells. However, Treg cell homeostasis, cell-type-specific gene expression and suppressive function critically depend on continuous triggering of their TCR.
