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Influence of dendritic cells on viral pathogenicity.

Freer G, Matteucci D - PLoS Pathog. (2009)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Retrovirus Center and Virology Section, Department of Experimental Pathology, University of Pisa, Pisa, Italy. freer@biomed.unipi.it

ABSTRACT
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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Related in: MedlinePlus

Viral patterns that activate the immune system.A virion can be envisioned as a concentration of different patterns recognized by the immune system: virtually all of its components can be used to start a response before the T cell compartment is active.
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ppat-1000384-g001: Viral patterns that activate the immune system.A virion can be envisioned as a concentration of different patterns recognized by the immune system: virtually all of its components can be used to start a response before the T cell compartment is active.

Mentions: Viruses are major targets of the immune system. A variety of viral 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 (see Figure 1). The integration of stimuli delivered by different viral 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” [1]. Like no other antigen-presenting cell, they can perform multiple immunogenic tasks, including i) priming of naïve 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 naïve 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 [2]. Indeed, the secretion of soluble mediators seems to be responsible for Th phenotype differentiation and is now considered “signal 3”, after MHC-peptide recognition (signal 1) and contact of costimulatory molecules (signal 2) [3]. The secretion of IL-12, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)- α is associated with skewing naïve T cells towards a Th1 phenotype, while Th2 cells are produced in the absence of such cytokines and in the presence of IL-10. In addition, transforming growth factor (TGF)-β induces Foxp3 and promotes the generation of CD25+ CD4+ T regulatory (Treg) cells, while IL-6 inhibits the generation of Treg cells and induces the production of T helper 17 (Th17) cells, suggesting another reciprocal developmental pathway for CD4+ T cells [4]. In turn, Treg cells hinder DCs and/or normal CD4+ T cells in their activities, while Th17 cells are involved in inflammatory and autoimmune reactions [5].


Influence of dendritic cells on viral pathogenicity.

Freer G, Matteucci D - PLoS Pathog. (2009)

Viral patterns that activate the immune system.A virion can be envisioned as a concentration of different patterns recognized by the immune system: virtually all of its components can be used to start a response before the T cell compartment is active.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2712770&req=5

ppat-1000384-g001: Viral patterns that activate the immune system.A virion can be envisioned as a concentration of different patterns recognized by the immune system: virtually all of its components can be used to start a response before the T cell compartment is active.
Mentions: Viruses are major targets of the immune system. A variety of viral 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 (see Figure 1). The integration of stimuli delivered by different viral 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” [1]. Like no other antigen-presenting cell, they can perform multiple immunogenic tasks, including i) priming of naïve 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 naïve 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 [2]. Indeed, the secretion of soluble mediators seems to be responsible for Th phenotype differentiation and is now considered “signal 3”, after MHC-peptide recognition (signal 1) and contact of costimulatory molecules (signal 2) [3]. The secretion of IL-12, IL-18, tumor necrosis factor (TNF)-α, and interferon (IFN)- α is associated with skewing naïve T cells towards a Th1 phenotype, while Th2 cells are produced in the absence of such cytokines and in the presence of IL-10. In addition, transforming growth factor (TGF)-β induces Foxp3 and promotes the generation of CD25+ CD4+ T regulatory (Treg) cells, while IL-6 inhibits the generation of Treg cells and induces the production of T helper 17 (Th17) cells, suggesting another reciprocal developmental pathway for CD4+ T cells [4]. In turn, Treg cells hinder DCs and/or normal CD4+ T cells in their activities, while Th17 cells are involved in inflammatory and autoimmune reactions [5].

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Retrovirus Center and Virology Section, Department of Experimental Pathology, University of Pisa, Pisa, Italy. freer@biomed.unipi.it

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus