2007
DOI: 10.1016/j.neulet.2007.04.071
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Japanese encephalitis virus infection decrease endogenous IL-10 production: Correlation with microglial activation and neuronal death

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Cited by 56 publications
(30 citation statements)
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“…IL-10 inhibits cytokine production by activated macrophages through Stat1 and Stat3 pathway (Fiorentino et al, 1991;O'Farrell et al, 1998). In brain, it has been shown that JEV infection causes decrease in IL-10 levels (Swarup et al, 2007a). We observed that IL-10 level was significantly reduced in JEV-infected macrophages, after 24 h of infection, but was increased after 72 h, as compared to control.…”
Section: Discussionmentioning
confidence: 45%
“…IL-10 inhibits cytokine production by activated macrophages through Stat1 and Stat3 pathway (Fiorentino et al, 1991;O'Farrell et al, 1998). In brain, it has been shown that JEV infection causes decrease in IL-10 levels (Swarup et al, 2007a). We observed that IL-10 level was significantly reduced in JEV-infected macrophages, after 24 h of infection, but was increased after 72 h, as compared to control.…”
Section: Discussionmentioning
confidence: 45%
“…IL-10 is a pleiotropic cytokine produced by T and B lymphocytes, macrophages, and microglia. Since this cytokine can directly limit accessory cell production of pro-inflammatory cytokines and prevent the up-regulation of co-stimulatory molecules, it is an important modulator of innate and adaptive immune responses (13). The role of cytokines is well known in neuro-infections.…”
Section: Discussionmentioning
confidence: 99%
“…CD4+ lymphocytes producing IL-12 stimulate the cytotoxic activity of CD8+ lymphocytes that arrive to the nervous tissue. These lymphocytes secrete proinflammatory mediators such as IFN-gamma, TNF-alpha and IL-6 that alter tissue homeostasis when expressed consistently during the infection (Chaturvedi et al, 2000;Sánchez-Burgos et al, 2004;Swarup et al, 2007). Additionally, CD8+ lymphocytes embedded in the tissue promote the death of both infected and uninfected cells via the release of perforin and granzymes and the expression of Fas ligand (FasL) (Courageot et al, 2003;Marques-Deak et al, 2005;Mellor & Munn, 2006;Rempel et al, 2004Rempel et al, , 2005.…”
Section: The Host Factor: Immune and Nervous Systemmentioning
confidence: 99%