Abstract
Recruitment of naturally occurring suppressive CD4(+), CD25(+), and FOXP3(+) regulatory T cells (T(reg)) to the tumor microenvironment (TME) has the potential to weaken the antitumor response in patients receiving treatment with immuno-oncology (IO) agents. Human T(reg) express CCR4 and can be recruited to the TME through the C-C chemokines CCL17 and CCL22. We have recently developed a series of potent, orally bioavailable small molecule antagonists of CCR4 that can block recruitment of T(reg) into the TME.