Abstract
The generation of a functional memory T cell pool upon primary encounter with an infectious pathogen is, in combination with humoral immunity, an essential process to confer protective immunity against reencounters with the same pathogen. A prerequisite for the generation and maintenance of long-lived memory T cells is the clearance of antigen after infection, which is fulfilled upon resolution of acute viral infections. Memory T cells play also a fundamental role during persistent viral infections by contributing to relative control and immuosurveillance of active replication or viral reactivation, respectively. However, the dynamics, the phenotype, the mechanisms of maintenance and the functionality of memory T cells which develop upon acute/resolved infection as opposed to chronic/latent infection differ substantially. In this review we summarize current knowledge about memory CD8 T cell responses elicited during α-, β-, and γ-herpes viral infections with major emphasis on the induction, maintenance and function of virus-specific memory CD8 T cells during viral latency and we discuss how the peculiar features of these memory CD8 T cell responses are related to the biology of these persistently infecting viruses.
Highlights
In the context of immunity, the notion of ‘memory’ refers to a property of the adaptive immune system to remember and recognize pathogens that have already infected the host in the past and to mount faster and stronger responses each time the same pathogen is encountered
We will focus our attention on the development and functional programming of memory CD8 T cells during persistent/latent viral infections, raising questions as to how continuous antigen stimulation shapes the memory CD8 T cell compartment, how the anatomical microenvironment of antigen presentation influence the state of memory and what role these memory CD8 T cells have in controlling viral latency
Cells, causing their accumulation or/and maintenance in the periphery (Figure 1C). In support of this hypothesis, using a chimeric system in which the expression of the H-2Kb molecule was restricted to immune-cells, we recently showed that inflation of the H-2Kb-restricted M38-specific CD8 T cell response was completely dependent on antigen presentation by non-hematopoietic cells [82]
Summary
In the context of immunity, the notion of ‘memory’ refers to a property of the adaptive immune system to remember and recognize pathogens that have already infected the host in the past and to mount faster and stronger responses each time the same pathogen is encountered. Many facets of T-cell functions at steady-state and during an immune response have been characterized, and, by the end of the 80s, the notion of T cell memory began to develop [3,4]. We will focus on memory CD8 T cells and how they adapt to the type of pathogen and to the anatomical localization to provide the host with best protection for any type of infection. We will focus our attention on the development and functional programming of memory CD8 T cells during persistent/latent viral infections, raising questions as to how continuous antigen stimulation shapes the memory CD8 T cell compartment, how the anatomical microenvironment of antigen presentation influence the state of memory and what role these memory CD8 T cells have in controlling viral latency
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