IP-10 is critical for effector T cell trafficking and host survival in Toxoplasma gondii infection.
The generation of an adaptive immune response against intracellular pathogens requires the recruitment of effector T cells to sites of infection. Here we show that the chemokine IP-10, a specific chemoattractant for activated T cells, controls this process in mice naturally infected with Toxoplasma gondii. Neutralization of IP-10 in infected mice inhibited the massive influx of T cells into tissues and impaired antigen-specific T cell effector functions. This resulted in >1000-fold increase in tissue parasite burden and a marked increase in mortality compared to control antibody-treated mice. These observations suggest that IP-10 may play a broader role in the localization and function of effector T cells at sites of Th1 inflammation.
Khan
I A
IA
Department of Medicine, Dartmouth Medical Center, Hanover, New Hampshire 03755, USA.
MacLean
J A
JA
Lee
F S
FS
Casciotti
L
L
DeHaan
E
E
Schwartzman
J D
JD
Luster
A D
AD
D000818:Animals; D002465:Cell Movement / Q000276:immunology; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000276:immunology*; D002630:Chemotactic Factors / Q000276:immunology; D007113:Immunity, Innate; D051379:Mice; D008810:Mice, Inbred C57BL; D013601:T-Lymphocytes / Q000276:immunology*; D014122:Toxoplasma / Q000276:immunology*; D014124:Toxoplasmosis, Animal / Q000276:immunology*
D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D002630:Chemotactic Factors