Karina Pino-Lagos

TL;DR: It is demonstrated that all-trans retinoic acid induces FoxP3+ adaptive T regulatory cells (A-Tregs) to acquire a gut-homing phenotype (α4β7+ CC chemokine receptor 9+) and the capacity to home to the lamina propria of the small intestine and indicates that RA production in vivo may drive both the imprinting and A-T Reg development in the face of overt inflammation.

TL;DR: The results obtained in this study establish that mast cells are essential in CD4+CD25+Foxp3+ regulatory T (TReg)-cell-dependent peripheral tolerance, and indicate that IL-9 represents the functional link through which activated TReg cells recruit and activate mast cells to mediate regional immune suppression.

TL;DR: It is shown that ex vivo splenic DCs are capable of inducing conversion of naïve CD4+ T cells to adaptive Foxp3+CD4+ regulatory T cells (aTreg) in the presence of TGF-β, and the CD8α+ DC subset were superior in inducing higher frequencies of conversion.

TL;DR: The authors propose that RA does not act directly on naive T cells during activation in culture but rather indirectly via negative regulation of an accompanying population of effector or memory CD4+ CD44hi cells, and show that RA is able to counterbalance the inhibitory effects of costimulation on TGF-β-mediated Foxp3 induction.

TL;DR: Immune cell activation induces concurrent temporal and spatial retinoic acid signaling, and CD4+ T cell–specific loss of RA signals reduces effector function, migration, and polarity.