We all know that CD4 regulatory T cells (Tregs) are required to maintain immunologic homeostasis and prevent autoimmunity and inflammatory lesions. Tregs express the transcription factor Foxp3, and can be divided into CD4+CD25+Foxp3+ thymus-derived, natural regulatory T cells (nTregs) and extrathymically induced Tregs (iTregs) that are derived in the periphery from CD4+CD25−Foxp3− precursors.
There is a huge lag in our knowledge as to the role of these two nTreg and iTreg subsets, and for instance we do not know whether they have separate or synergistic roles in vivo.
Alexandre Rudensky and colleagues have developed a model system that allows to specifically knock-down the development of peripheral iTreg. Indeed, they had previously shown (see Nature, 2010, 463(7282):808-12) that deletion in mice of a CNS1 present in the Foxp3 gene, that is critical for TGFβ-dependent induction of Foxp3, provokes the selective impairment of peripheral iTreg differentiation.
Using this model, they now show that the absence of peripheral iTreg results in spontaneous allergic Th2 type inflammation in the intestine and lungs. This is the first demonstration of a selective role for peripheral iTreg in vivo! Thus, if you want to read more here is the link iTreg control Th2 cells!