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• W1965931837 abstract "We previously reported a requirement of interferon-γ (IFN-γ) production by both T cells and cells other than T or natural killer (NK) cells in the brain for prevention of toxoplasmic encephalitis. In the present study, we examined whether microglia, the resident macrophage system in the brain, produce IFN-γ in response to infection with Toxoplasma gondii in SCID and wild-type BALB/c mice. IFN-γ was detected in the culture supernatants of microglia purified from the brains of SCID mice that had developed toxoplasmic encephalitis due to reactivation of infection. A significant increase in numbers of IFN-γ-expressing microglia was also observed by immunostaining for this cytokine in the brains of SCID and BALB/c mice during the acute stage of acquired infection, and those numbers decreased in the later stage of infection in the BALB/c animals. These results indicate that microglia produce IFN-γ in the presence and absence of T cells in response to reactivated or acute acquired infection in the brain. Because IFN-γ is the essential effector molecule to control tachyzoites and because this cytokine is a potent inducer of expression of chemokines and MHC antigens important for recruitment and activation of T cells, IFN-γ production by microglia might play a critical role in the early stage of tachyzoite proliferation in the brain by limiting parasite growth and initiating subsequent T cell immunity." @default.
• W1965931837 created "2016-06-24" @default.
• W1965931837 creator A5025887775 @default.
• W1965931837 creator A5073588329 @default.
• W1965931837 date "2007-07-01" @default.
• W1965931837 modified "2023-10-17" @default.
• W1965931837 title "Microglia Produce IFN-<i>γ</i>Independently from T Cells During Acute Toxoplasmosis in the Brain" @default.
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• W1965931837 doi "https://doi.org/10.1089/jir.2006.0157" @default.
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