Abstract
Marek’s disease (MD) is a lymphoproliferative disease in chickens caused by Marek’s disease virus (MDV), a highly oncogenic alphaherpesvirus. Since 1970, MD has been controlled through widespread vaccination of commercial flocks. However, repeated and unpredictable MD outbreaks continue to occur in vaccinated flocks, indicating the need for a better understanding of MDV pathogenesis to guide improved or alternative control measures. As MDV is an intracellular pathogen that infects and transforms CD4+ T cells, the host cell-mediated immune response is considered to be vital for controlling MDV replication and tumor formation. In this study, we addressed the role of CD8+ T cells in vaccinal protection by widely-used monovalent (SB-1 and HVT) and bivalent (SB-1+HVT) MD vaccines. We established a method to deplete CD8+ T cells in chickens and found that their depletion through injection of anti-CD8 monoclonal antibodies (mAb) increased tumor induction and MD pathology, and reduced vaccinal protection to MD, which supports the important role of CD8+ T cells for both MD and vaccinal protection.
Highlights
The cytotoxic T-lymphocyte (CTL) response generated from activated CD8+ T cells is an effective immune response that combats infectious pathogens [1]
We investigated the effect of CD8+ T cells on both Marek’s disease (MD) incidence and vaccinal protection
We provided evidence that CD8+ T cells are important for MD protection and prevention in both unvaccinated as well as vaccinated chickens
Summary
The cytotoxic T-lymphocyte (CTL) response generated from activated CD8+ T cells is an effective immune response that combats infectious pathogens [1]. CTL response functions by recognizing foreign antigens presented by MHC class I of infected cells, destroying the cells by releasing perforin and granzyme to induce apoptosis. CD8+ T cells produce and secrete cytokines, such as IFN-γ that directly inhibits viral replication, induces maturation of macrophages, and activates the natural killer (NK) cell response. CD8+ effector cells can secrete chemokines to further prolong the CD8 T cell response.
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