Miao-Tzu Huang and Bor-Luen Chiang
Since the characterization of CD4+CD25+ regulatory T cells (Tregs) as a specific T-cell lineage with immune regulatory function in the 1990s, approaches manipulating Treg expansion and activities have been proved potential therapeutic strategies for immune-mediated diseases. On the other hand, harnessing leukocyte migration during inflammation as a therapeutic modality for immunologic diseases has not only supported by theoretical basis but also clinically shown potential. Whilst advances have been made in the understanding of the effector mechanisms of Treg-mediated immune suppression, the migration phenotypes as well as the anatomic sites where Tregs exert immune regulation remain obscured.
In a recent study by using the foot-pad inflammation model and adoptive Treg-cell transfer, Huang et al. demonstrated that blockage of Treg lymph node localization abrogated the immune suppressive function of Tregs, suggesting an indispensable role of lymph node trafficking in Treg-mediated immune regulation. Important messages have arisen from this study that migration pattern, i.e. lymph node localization vs. tissue trafficking, matters in the context of Treg-mediated immune regulation and Treg-based cell therapy.
Whilst inflammatory response can be regulated by modulating the migration property of inflammatory leukocytes and be a feasible therapeutic modality, the impact of altered Treg migration phenotypes on the overall inflammatory outcome and the effectiveness of therapy of this kind should be taken into account.