Key points are not available for this paper at this time.
Significance The current study identifies CCR8 + regulatory T cells (T reg cells) as drivers of immunosuppression and provides compelling evidence of a self-feeding mechanism by which, at an autoimmune site, CCL1 produced by FOXp3 + T reg cells upregulates the expression of its own receptor, CCR8, on these cells, and potentiates their in vivo proliferation and suppressive activities as driver T reg cells. The suppression of ongoing autoimmunity by a stabilized version of the chemokine (CCL1–Ig) highlights the translational potential of these findings.
Barsheshet et al. (Mon,) studied this question.