Key result
Neutralization of gamma interferon interferes with MHC class II-dependent antigen presentation and CD4+ T cell proliferation, leading to susceptibility to measles virus-induced encephalitis.
In a mouse model of measles virus encephalitis, gamma interferon protects by stimulating MHC class II-dependent antigen presentation and CD4+ T cell proliferation rather than through direct antiviral effects.
Should not alter clinical approaches to measles encephalitis; leaves open IFN-γ mechanisms in human viral CNS disease.
BALB/c mice are resistant to measles virus (MV)-induced encephalitis due to their strong MV-specific CD4(+) T-cell response. Resistance is broken by neutralization of gamma interferon with monoclonal antibodies, indicating an important role for this pleiotropic cytokine. Here, we demonstrate that mouse gamma interferon has no direct antiviral effect in vitro and in vivo. The breakdown of resistance is due neither to a switch in the T-helper response nor to an impaired migration of CD4(+) T cells. Neutralization of gamma interferon interferes with the major histocompatibility complex class II-dependent antigen presentation and subsequent proliferation of CD4(+) T cells in vitro and in vivo. In consequence, the reduction in numbers of CD4(+) T cells below a protective threshold leads to susceptibility to MV-induced encephalitis.
No takes yet. Share an insight, caveat, or question.
Weidinger et al. (2001) studied Measles Virus-Induced Encephalitis. Neutralization of gamma interferon vs. Untreated controls was evaluated on MHC class II-dependent antigen presentation and CD4+ T cell proliferation. Neutralization of gamma interferon interferes with MHC class II-dependent antigen presentation and CD4+ T cell proliferation, leading to susceptibility to measles virus-induced encephalitis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: