Table 2.

Inhibitory receptors that mediate Tregs inhibitory effects.

Inhibitory receptors	Effects	References
CTLA-4	Blocking the subsequent increase of CD80 and CD86 expression and down-regulates the expression of CD80 and CD86 Decreasing the antigen presentation ability of DCs Promoting the secretion of suppressive factors (i.e. IDO) by DCs	(11, 38)
Nrp-1	Increasing interaction of Tregs with DCs Decreasing antigen presentation in DCs	(11, 81)
Galectin-1	Plays an important role in Treg-DC or Treg-T cell interactions Cell cycle arrest in effector T cells and DCs Inducing apoptosis in effector T cells and DCs Inhibit proinflammatory cytokines production	(11, 38, 82)
LAG-3	Preventing DC maturation Reducing DC antigen presentation capability Suppressing effector T cells	(11, 38)
CD39	Ectonucleotidase enzyme that hydrolyses ATP or ADP to AMP AMP Allows the Tregs to enter inflamed regions and allow the Tregs decreasing ATP-driven proinflammatory processes in different cell types, particularly DCs	(38, 83)
CD73	Turning AMP to adenosine Adenosine: Inhibits the functions of DCs as well as effector T cells Down-regulates NF-κB activation in effector T cells Reducing the release of many proinflammatory cytokines and chemokines from effector T cells Increasing expansion of Tregs Increasing immunoregulatory activity of Tregs	(38, 47, 50, 84)

CTLA-4, cytotoxic T lymphocyte-associated antigen-4; LAG3, lymphocyte activation gene 3; Nrp-1, Neuropilin.