TY - JOUR
T1 - Microglia produce IFN-γ independently from T cells during acute toxoplasmosis in the brain
AU - Wang, Xisheng
AU - Suzuki, Yasuhiro
PY - 2007/7
Y1 - 2007/7
N2 - 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.
AB - 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.
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U2 - 10.1089/jir.2006.0157
DO - 10.1089/jir.2006.0157
M3 - Article
C2 - 17651021
AN - SCOPUS:34547201936
SN - 1079-9907
VL - 27
SP - 599
EP - 605
JO - Journal of Interferon and Cytokine Research
JF - Journal of Interferon and Cytokine Research
IS - 7
ER -