Chronic Viral Infections Interfere with the Activation of CD8+T Cells

Abstract

To optimally prime naïve CD8+ T cells pAPCs, such as dendritic cells and macrophages, must present appropriate viral
peptides to CD8+ T cells. Priming of CD8+T cells can be either via direct presentation by using endogenous antigens
or cross-presentation by utilizing exogenous antigens. Licensing of pAPCs to activate CD+T cells are greatly affected
by infection with some viruses that interfere with pathways of antigen presentation. In our results, LCMV-infected
macrophages have upregulated their phagocytic activity up to 2 folds than normal, in vitro. Besides, BM-MØ prepared
from LCMV-WE and Cl13-infected mice have shown an interesting variation in up-regulating some surface markers.
Importantly, while LCMV-Cl13 has increased CD86 expression rates, LCMV-WE had no effect. Additionally, BM- MØ
derived from LCMV-WE and Cl13-infectd mice have activated LCMV-specific CD8+T cells equally. In contrast, Sp-MØ
prepared from LCMV-WE, but not from LCMV-Cl13-infected mice, have lost their ability to activate the same CD8+T cells
profile. In other hand, cross-priming of OVA-specific CD8+T cells was greatly affected by subjecting mice to LCMV-WE
and Cl13 infection. While LCMV-WE improved the cross-priming efficiency of OVA-specific CD8+T cells, LCMV-Cl13
downregulated the cross-priming efficiency of OVA-specific CD8+T cells. Collectively, induction of CD8+T cells to exert
their cytotoxic activity against infection, via either direct or cross- presentation pathways, is greatly influenced by acute vs.
chronic virus infection.