TY - JOUR
AU - Sacks, David L.
AB - The long-term persistence of pathogens in a host that is also able to maintain strong resistance to reinfection, referred to as concomitant immunity, is a hallmark of certain infectious diseases, including tuberculosis and leishmaniasis. The ability of pathogens to establish latency in immune individuals often has severe consequences for disease reactivation
1,2,3
. Here we show that the persistence of Leishmania major in the skin after healing in resistant C57BL/6 mice is controlled by an endogenous population of CD4+CD25+ regulatory T cells. These cells constitute 5–10% of peripheral CD4+ T cells in naive mice and humans, and suppress several potentially pathogenic responses in vivo, particularly T-cell responses directed against self-antigens
4
. During infection by L. major, CD4+CD25+ T cells accumulate in the dermis, where they suppress—by both interleukin-10-dependent and interleukin-10-independent mechanisms—the ability of CD4+CD25- effector T cells to eliminate the parasite from the site. The sterilizing immunity achieved in mice with impaired IL-10 activity is followed by the loss of immunity to reinfection, indicating that the equilibrium established between effector and regulatory T cells in sites of chronic infection might reflect both parasite and host survival strategies.
TI - CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity
JF - Nature
DO - 10.1038/nature01152
DA - 2002-12-05
UR - https://www.deepdyve.com/lp/springer-journals/cd4-cd25-regulatory-t-cells-control-leishmania-major-persistence-and-dCkh2qpPQW
SP - 502
EP - 507
VL - 420
IS - 6915
DP - DeepDyve
ER -