Journal
IMMUNITY
Volume 12, Issue 5, Pages 483-494Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(00)80200-9
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Funding
- NCI NIH HHS [CA69212] Funding Source: Medline
- NIAID NIH HHS [AI46999, AI33325] Funding Source: Medline
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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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