|OCHIAI, ERI - University Of Kentucky|
|BROGLI, MORGAN - University Of Kentucky|
|KUDO, TOMOYA - University Of Kentucky|
|WANG, XISHENG - University Of Kentucky|
|SUZUKI, YASUHIRO - University Of Kentucky|
Submitted to: American Journal of Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/20/2015
Publication Date: 2/20/2015
Citation: Ochiai, E., Brogli, M., Kudo, T., Wang, X., Dubey, J.P., Suzuki, Y. 2015. CXCL9 Is Important for Recruiting Immune T Cells into the Brain and Inducing an accumulation of the T Cells to the areas of tachyzoite proliferation to prevent reactivation of chronic cerebral infection with Toxoplasma gondii. American Journal of Pathology. 185(2):314-24.
Interpretive Summary: Toxoplasmosis continues to be a major public health problem in the US. The single celled parasite, Toxoplasma gondii, causes abortion in livestock and mental retardation in children. Approximately 30% of adult humans in the US have been exposed to this parasite. Toxoplasmosis is asymptomatic in most adult persons but it can be lethal in those with immnuedeficiencies such as persons with AIDS or those on immunotherapy for transplant or cancer treatment. In these patients the dormant parasite is reactivated resulting in destruction of tissues. The mechanism for reactivation is not fully understood. In the present papers authors explain the mechanism of reactivation of infection. Most persons infected with this This finding will be of interest to Parasitologists, immunologists, and scientists in general.
Technical Abstract: T cells are required to maintain the latency of chronic infection with Toxoplasma gondii in the brain. In the present study, we examined the role of non-ELR (glutamic acid-leucine-arginine) CXC chemokine CXCL9 for T cell recruitment to prevent reactivation of infection with T. gondii. SCID mice were infected and treated with sulfadiazine to establish a chronic infection. Immune T cells from infected wild-type mice were transferred into the animals in combination with treatment with anti-CXCL9 or control sera. Three days later, sulfadiazine was discontinued to initiate reactivation of infection. Numbers of CD4+ and CD8+ T cells isolated from the brains were markedly less in mice treated with anti-CXCL9 serum than those treated with control serum at 3 days after sulfadiazine discontinuation. Amounts of tachyzoite(acute stage form of T. gondii)-specific SAG1 mRNA and numbers of foci associated with tachyzoites were significantly greater in the former than the latter at 5 days after sulfadiazine discontinuation. An accumulation of CD3+ T cells into the areas of tachyzoite growth was significantly less frequent in the animals treated with anti-CXCL9 serum than those treated with control serum. These results indicate that CXCL9 is crucial for recruiting immune T cells into the brain and inducing an accumulation of the T cells into the areas where tachyzoites proliferate to prevent reactivation of chronic T. gondii infection.