Cutting edge: murine CD59a modulates antiviral CD4+ T cell activity in a complement-independent manner.

CD59a deficiency exacerbates influenza-induced lung inflammation through complement-dependent and-independent mechanisms

Influenza-specific immune activity not only promotes virus clearance but also causes immunopathology, thereby underlining the importance of mounting a measured anti-viral immune response. Since complement bridges both the innate and adaptive immune systems and has been implicated in defence against influenza, the role of the complement regulator CD59a in modulating the response to influenza was...

Antiviral Cd4 T Cell Response Il-2 Signaling Is Sustained during Early Cutting Edge: Paracrine, but Not Autocrine

Memory CD4+ T-cell-mediated protection from lethal coronavirus encephalomyelitis.

The antiviral role of CD4(+) T cells in virus-induced pathologies of the central nervous system (CNS) has not been explored extensively. Control of neurotropic mouse hepatitis virus (JHMV) requires the collaboration of CD4(+) and CD8(+) T cells, with CD8(+) T cells providing direct perforin and gamma interferon (IFN-gamma)-mediated antiviral activity. To distinguish bystander from direct antivi...

Response Induces a Polyfunctional CD4 T Cell Cutting Edge: Murine Cytomegalovirus

Cutting edge: activation of virus-specific CD4 T cells throughout γ-herpesvirus latency.

CD4 T cells are essential for immune control of γ-herpesvirus latency. We previously identified a murine MHC class II-restricted epitope in γ-herpesvirus-68 gp150 (gp150(67-83)I-A(b)) that elicits CD4 T cells that are maintained throughout long-term infection. However, it is unknown whether naive cells can be recruited into the antiviral CD4 T cell pool during latency. In this study, we generat...