[HTML][HTML] 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 …
E Ochiai, Q Sa, M Brogli, T Kudo, X Wang… - The American journal of …, 2015 - Elsevier
E Ochiai, Q Sa, M Brogli, T Kudo, X Wang, JP Dubey, Y Suzuki
The American journal of pathology, 2015•ElsevierT cells are required to maintain the latency of chronic infection with Toxoplasma gondii in the
brain. Here, we examined the role of non–glutamic acid-leucine-arginine CXC chemokine
CXCL9 for T-cell recruitment to prevent reactivation of infection with T. gondii. Severe
combined immunodeficient (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 SCID mice in combination with treatment with anti-CXCL9 or control sera. Three …
brain. Here, we examined the role of non–glutamic acid-leucine-arginine CXC chemokine
CXCL9 for T-cell recruitment to prevent reactivation of infection with T. gondii. Severe
combined immunodeficient (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 SCID mice in combination with treatment with anti-CXCL9 or control sera. Three …
T cells are required to maintain the latency of chronic infection with Toxoplasma gondii in the brain. Here, we examined the role of non–glutamic acid-leucine-arginine CXC chemokine CXCL9 for T-cell recruitment to prevent reactivation of infection with T. gondii. Severe combined immunodeficient (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 SCID mice 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 in mice 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 SCID mice treated with anti-CXCL9 serum than in mice 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.
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