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Abstract
Memory T cells are a fundamental component of immunological memory, providing rapid and potent host protection against secondary challenges. As such, memory T cells are key targets in the design of vaccination strategies and cancer immunotherapies, making it critical to understand the factors and mechanisms that regulate their biology. Diet is an environmental feature that impacts virtually all aspects of host physiology. However, the influence of specific dietary regiments and nutritional components on the immune system is only just starting to be uncovered. This article will review literature regarding the impact of diet and nutrition on memory T cell development, maintenance and function. It was recently shown that caloric restriction without undernutrition enhances memory T cell function, while diets high in fiber are also beneficial. However, memory T cell responses are dysfunctional in extreme nutritional states, such as undernutrition and diet-induced obesity. Therefore, diet and host nutritional status are major regulators of memory T cell biology and host fitness. To define the dietary balance required to promote optimal memory T cell responses could allow for the implementation of rational diet-based therapies that prevent or treat disease. Furthermore, that certain dietary regiments can enhance memory T cell function indicates the possibility of harnessing the underlying mechanisms in the design of novel vaccination strategies and cancer immunotherapies.
Highlights
Antigen-specific naïve T cells interact with antigen-presenting cells displaying cognate antigen in the context of major histocompatibility molecules, resulting in extensive T cell proliferation and the acquisition of an effector program [1]
Memory T cells have traditionally been partitioned into subsets based on migratory capacity and type of effector functions exhibited upon secondary challenge [1,2]
Several lines of research support the notion that Caloric restriction (CR) promotes memory T cell function to mediate host protection against secondary challenges, which may be regulated by the mechanistic target of rapamycin (mTOR) pathway
Summary
Antigen-specific naïve T cells interact with antigen-presenting cells displaying cognate antigen in the context of major histocompatibility molecules, resulting in extensive T cell proliferation and the acquisition of an effector program [1]. Memory T cells have traditionally been partitioned into subsets based on migratory capacity and type of effector functions exhibited upon secondary challenge [1,2]. Tissue-resident memory T cells (TRM) are non-migratory, persisting long-term in tissues without re-entering the circulation [2] These cells rapidly produce cytokines that initiate and amplify local immune responses, thereby providing exposed sites with an essential layer of protection [2,4,5,6]. The host is likely to be exposed to a fluctuating environment over time, with alterations in caloric intake and dietary composition a common occurrence throughout evolutionary history How such events impact the immune system and the memory T cell compartment are just beginning to be characterized [22,23,24]
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