The influence of dendritic cells on virus pathogenicity

Dendritic cell Viruses are major targets of the immune system. A variety of virus pathogen-associated molecular patterns (PAMPs), such as the high repetition of capsomers and/or peplomers on virion surface, the production of unique RNA replication intermediates and genome modifications, and others, are recognized as markers of viral invasion by responsive molecules on immune effector cells. The integration of stimuli delivered by different virus PAMPs leads to inflammation and immune activation which, in turn, are key components of both pathogenesis and recovery from viral infection.

Dendritic cells (DCs) possess properties and abilities enabling them to act as unique immune “live adjuvants”. Like no other antigen-presenting cell, they can perform multiple immunogenic tasks, including i) priming of naive T cells by the expression of special costimulatory surface molecules; ii) cross-presentation, that is, presentation of exogenous antigens in the context of MHC class I molecules to CD8+ T lymphocytes, in addition to presentation of MHC class II-restricted peptides; and iii) polarizing naive T cells to various Th phenotypes. DC activity is normally triggered by pathogens via a variety of receptor molecules and includes the release of distinct interleukins (ILs) directed at regulating T cell differentiation.

Influence of Dendritic Cells on Viral Pathogenicity. 2009 PLoS Pathog 5(7): e1000384 doi:10.1371/journal.ppat.1000384
Although most viral infections cause minor, if any, symptoms, a certain number result in serious illness. Viral disease symptoms result both from direct viral replication within host cells and from indirect immunopathological consequences. Dendritic cells (DCs) are key determinants of viral disease outcome; they activate immune responses during viral infection and direct T cells toward distinct T helper type responses. Certain viruses are able to skew cytokine secretion by DCs inducing and/or downregulating the immune system with the aim of facilitating and prolonging release of progeny. Thus, the interaction of DCs with viruses most often results in the absence of disease or complete recovery when natural functions of DCs prevail, but may lead to chronic illness or death when these functions are outmanoeuvred by viruses in the exploitation of DCs.

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