IP-10 is critical for effector T cell trafficking and host survival in Toxoplasma gondii infection
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Khan, IA
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机构:Harvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USA
Khan, IA
MacLean, JA
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机构:Harvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USA
MacLean, JA
Lee, FS
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机构:Harvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USA
Lee, FS
Casciotti, L
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Casciotti, L
DeHaan, E
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DeHaan, E
Schwartzman, JD
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Schwartzman, JD
Luster, AD
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Harvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USAHarvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USA
Luster, AD
[1
]
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[1] Harvard Univ, Massachusetts Gen Hosp, AIDS Res Ctr, Sch Med,Allergy & Immunol Unit,Infect Dis Unit, Boston, MA 02114 USA
[2] Dartmouth Med Ctr, Dept Med, Hanover, NH 03755 USA
[3] Dartmouth Med Ctr, Dept Pathol, Hanover, NH 03755 USA
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.
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页码:483 / 494
页数:12
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