Abstract
Pre-existing T cell memory provides substantial protection against viral, bacterial, and parasitic infections. The generation of protective T cell memory constitutes a primary goal for cell-mediated vaccines, thus understanding the mechanistic basis of memory development and maintenance are of major importance. The widely accepted idea that T cell memory pools are directly descended from the effector populations has been challenged by recent reports that provide evidence for the early establishment of T cell memory and suggest that the putative memory precursor T cells do not undergo full expansion to effector status. Moreover, it appears that once the memory T cells are established early in life, they can persist for the lifetime of an individual. This is in contrast to the reported waning of naïve T cell immunity with age. Thus, in the elderly, immune memory that was induced at an early age may be more robust than recently induced memory, despite the necessity for long persistence. The present review discusses the mechanisms underlying the early establishment of immunological memory and the subsequent persistence of memory T cell pools in animal models and humans.
Highlights
Memory T cells provide protection against re-infection with the same pathogen enabling a more rapid recovery of the host and a milder clinical outcome (Powell et al, 2007)
The future design of T cell-based vaccination strategies that can provide effective and optimal protection across the lifespan of an individual crucially depends upon an in-depth understanding of the development and maintenance of T cell memory and the factors that impact the protective capacity of memory T cell populations
Studies in recent years have made substantial progress in dissecting the complexities of T cell memory populations, resulting in the identification of major factors that influence the composition and stability of these T cell memory populations. While these advances have moved us closer to elucidating the mechanisms contributing to optimal T cell memory generation, there remain many aspects of T cell memory to be investigated
Summary
Memory T cells provide protection against re-infection with the same pathogen enabling a more rapid recovery of the host and a milder clinical outcome (Powell et al, 2007). A seminal paper by Sallusto et al (1999) coined the terms “central” (CD62Lhi) and “effector” (CD62Llo) to describe these memory T cell subsets These findings challenged the traditional view of memory formation, suggesting a more complex process, and raised important questions about the generation of T cell memory and which populations persist for the life-time of an individual. More than a decade of research and published studies provide evidence of the early establishment of memory, which can be greatly affected by the inflammatory stimuli and transcription signatures at the acute phase of the infection Both animal and human studies show that T cell memory is long-lived and can be detected for up to 75 years in humans (Hammarlund et al, 2003) and for the life-time of a laboratory mouse (Valkenburg et al, 2012). We discuss both the establishment and persistence of primary T cell memory, with a particular focus on CD8+ T cell responses directed at acute readily resolved infections such as respiratory viruses
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