Abstract
Advanced age is associated with a declining ability to mount satisfactory immune responses (i.e. immunosenescence) resulting in increased infection susceptibility and diminished vaccine-elicited immune responses. Paradoxically, aged individuals also have a reduced ability to resolve certain types of inflammation (i.e. inflammaging) leading to chronic, low-grade inflammatory responses and the development of inflammation-associated comorbidities, such as cardiovascular disease, autoimmunity, and malignancy. The contribution of immunosenescence and inflammaging to human disease is substantial, thus highlighting the importance of understanding the mechanisms responsible for these processes.
Highlights
Advanced age is associated with a declining ability to mount satisfactory immune responses resulting in increased infection susceptibility and diminished vaccine-elicited immune responses
T follicular helper (Tfh) cells have been implicated in the regulation of chronic inflammation, and our recent study suggests that this may include inflammaging [1]
These endogenous, small RNAs exert their effect through the post-transcriptional modification of messenger RNA and are essential for an array of normal and aberrant biological processes [6]. miR-146a and miR-155 are among the microRNAs shown to be key mediators of the immune response. miR-155 is a potent pro-inflammatory enhancer that is induced by a variety of Toll-like receptor ligands, cytokines, and antigens, whereas miR146a functions as a safeguard against autoimmunity and promotes resolution of the inflammatory response by limiting activation of T cells [7]. miR-146a-/- mice undergo an age-dependent decrease in life expectancy due to severe immune dysfunction and the development of hematopoietic tumors, malignancy, and inflammation within secondary lymphoid organs
Summary
Advanced age is associated with a declining ability to mount satisfactory immune responses (i.e. immunosenescence) resulting in increased infection susceptibility and diminished vaccine-elicited immune responses. T follicular helper (Tfh) cells have been implicated in the regulation of chronic inflammation, and our recent study suggests that this may include inflammaging [1]. Despite a flurry of new information about the multifaceted roles of Tfh cells and molecular mechanisms that regulate their biology, additional gaps exist in our understanding of their differentiation and their roles in inflammatory conditions.
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